Chronic Disease Part 4: Type 2 Diabetes – Part 1

Let’s start with a story…

Man on a Train

I was exiting a train on the platform at Reagan Airport when suddenly I see a man falling back onto the train as it was pulling away. His eyes were rolled back and he looked limp. My husband and I pulled him off the moving train that was starting to carry him down the platform. He was somewhat conscious, enough to get a faint mumbled medical history which included diabetes. He swore he had eaten this morning, just an apple, but he knew his blood sugar was fine. I checked him for injuries and monitored him until first responders arrived.

I passed on the history of diabetes to the first responders. Their first task was to take his blood glucose. It was in the 30s. His apple had not been enough or there had been some issue with his medications and he was tanking fast. I had some candy, so we gave him that, and they took him away in the ambulance.

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I feel like Physical Therapists should be on the front line providing treatment for diabetes. Yes, I said front line, and yes, I said treatment (and I’m not alone in that!). And not just because up to 80% of the patients referred to us HAVE some type of diabetes! But, we have definitely not positioned ourselves this way. We currently treat diabetes as a comorbidity, when really it’s almost always the primary concern.

Diabetic with a broken leg? Diabetic changes to the blood vessels resulted in poor nutrient circulation to bone tissue resulting in decreased bone quality.

Diabetic with cancer? Systemic declines in immune function secondary to diabetic changes reduced the ability to fend off cancer.

Diabetic with a wound (even a surgical wound)? Healing is going to take twice as long, if not more because diabetic changes to the tissues and vessels will reduce the ability to heal. Diabetes may have even caused the wound to start with!

Diabetic with a frozen shoulder? Don’t even get me started…

So, why don’t Physical Therapists position themselves to treat diabetes? Well, it’s pretty hard to make exercise sound like a better treatment than taking a single Metformin every day… But, I’m here to give it my darndest.

Managing Type 2 Diabetes

Blood glucose monitoring. Your ability to do this may vary based on your state, but we all know the importance of blood glucose levels for exercise. If we don’t time our sessions properly, we end up with a patient passing out on us. If we do time them properly, we can actually (over time) decrease or eliminate the need for medication to manage blood glucose. Let’s talk about the logistics of this:

  1. To clear up the risk analysis: If your patient is already diabetic, they already have a physician’s order to check their blood glucose daily. If you ask them to or assist them in doing this prior to your session or during your session, you are in full compliance with this order. If you need to do this for your patient because they are unable, you are still in full compliance with this order. If your patient’s blood glucose is so low that they are unable to measure their own blood glucose, are you going to sit there wondering if it’s ok while they fade away? No, of course not. You should probably be calling 911 at that point, but take their blood glucose. (Side note: please wear gloves.) Diabetic teaching is well within our scope of practice. So is diabetic intervention (aka exercise). PTs can even become certified diabetic educators.
  2. You cannot administer insulin if your patient’s blood glucose is too high unless you are trained to use the devices to do so and there is an order in place (if your patient is diabetic, there is an order in place, but you have to know how much, i.e. sliding scales and all that). You should be calling the physician or nurse case manager for instruction if your patient cannot self-administer. You can, on the opposite end of the spectrum, give your patient food. You should have fast-acting sugars available in your clinic: juice, candy, applesauce… Even in outpatient clinics, I’ve given juice when I noticed the signs of hypoglycemia.
  3. You, yes YOU, a rehab clinician, can educate patients on diet, how to use a glucometer, and how to use a sliding scale. It is within the scope of practice of a physical therapist to educate on medications as the primary case manager under Medicare guidelines. If you can do an OASIS, you can teach meds. As a matter of fact, it is EXPECTED that you complete the meds teaching to the best of your ability and consult nursing for the rest. Sliding scales are provided for you by the primary care physician or endocrinologist, so you just explain how to use them. If you aren’t sure, check out some online training courses to get more information.
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Not My Patient

I made a home visit to evaluate a very kind woman who did not want my help. She wasn’t rude, she was just straightforward. As her doctor did order PT for falls, I talked her into letting me do a walk around the house with her.

It wasn’t her house, she told me. She was just staying with family for a while until she felt better. We walked through a few rooms and saw a few different people. It wasn’t their house either, she explained. Her family takes in people who need some help until they can get back home. She was walking fine without a device, albeit a bit slow over the changing carpets in this piece-meal home.

We passed by a bedroom where her sister-in-law was shaking a man lying in bed. The woman was audibly yelling at the man who was only somewhat mumbling back to her. I sat back down at the dining table with my patient who clearly told me she was fine. And then I hear the words from the other room…

“530? What does that mean? What’s his sugar supposed to be?”

I smiled at my patient and said, “if you don’t want me to come to see you, that’s fine with me. That man right there is in trouble. Would you mind if I helped him?” She smiled and said, “of course, honey, he’s been real sick.”

I ran to the room and did a recheck on the glucose. The 530 was just the most recent on the glucometer history. The actual was 615. He was losing consciousness when I called 911. The family gave me a first name and age but I had no other medical information. The paramedics were quick to arrive and stretchered him quickly to the ambulance.

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What ARE the signs of hypoglycemia?

I’m so glad you asked!

  1. Arrhythmia
  2. Fatigue
  3. Palor
  4. Sweating
  5. Anxiety/mood changes
  6. Confusion
  7. Lightheadedness/headache
  8. Shaking
  9. Unsteadiness
  10. Anxiety

And one list is not complete without the other…

What are the signs of hyperglycemia?

  1. Fatigue
  2. Weakness
  3. Confusion
  4. Nausea/vomiting
  5. Shortness of breath
  6. Dry mouth/fruity breath
  7. Urinary frequency
  8. Headache
  9. Blurry vision

Now look at those two lists… lots of similarities there… so it may be difficult to actually tell if your patient is hyper or hypoglycemic. This is why you will need to check their blood glucose.

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The Need to Know

Just like with pulse oximetry for patients with respiratory conditions, blood glucose in people with diabetes is something I NEED to know. I need to know what it is before exercise, what the trends are, and what it is first thing in the morning. That’s how I know if the diabetes is well-managed or not and determines how and when I prescribe exercise.

What are safe parameters for blood glucose?

I thought you’d never ask! Here’s the meat and potatoes. Let’s put these numbers in order from least to most and make a scale. Remember, these numbers assume the person already has a diagnosis of type 2 diabetes.

Too Low

<50 mg/dL
call physician/911 based on symptoms,
give sugar

Too Low for Exercise

<70 mg/dL,
give sugar

Ideal Range for Exercise

100 – 250mg/dL

Too High for Exercise

>250 mg/dL call physician, risk of ketoacidosis

Too High

>350 mg/dL call physician/911 based on symptoms

If a patient with diabetes is participating in an exercise class or performing exercise in long bouts (longer than 60 minutes) blood glucose should be checked every 30 minutes to ensure ongoing safety to reduce the risk of ketoacidosis or hypoglycemia. Ketoacidosis is when there are too many ketones in the body. For diabetic people, this can be life-threatening. But, that’s a whole other condition, so we will talk about that later. Just know that it is a medical emergency and refer to my friend above who wasn’t my patient.

Effects of exercise (which are many!) on blood glucose only last 24 hours, so some type of exercise should be performed EVERY day for long-term stabilization and management. And, as I usually make the statements about properly prescribed exercise, that all applies here, too. Set a baseline exercise tolerance or aerobic capacity, measure vitals, calculate heart rates, and exercise to the proper ranges. Not only will this help manage blood-glucose long-term, but it will help reduce pain associated with peripheral vascular changes due to diabetes, too.

Don’t Forget Diet

Nutritional counseling is well within our scope of practice as rehab providers, especially if our patients are diabetic. It isn’t even safe for our patients to exercise without knowing the basics of how energy input and energy output affect their health status.

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Don’t be shocked if your patient doesn’t know where sugar comes from, what carbs are, or if bread is a protein or not (very serious, I had that exact conversation once). Some people take it upon themselves to know a lot about their health and what they can do to manage it, but many people don’t. Their health is something that happens to them, not something they actively participate in. So, it will take a lot of counseling to get their energy inputs and outputs back on track.

Don’t forget to call on your handy dandy dietician, too. Diabetes takes a team. Hopefully, you are on that team and can help the patient balance those energy inputs and outputs and keep them safe while you do it.

Keep in mind that the more comorbidities your patient has, the harder it will be to control their diabetes. Many medications and other conditions impact blood glucose and just throw the whole thing off! Goodness, so much to cover and we haven’t even gotten to the feet yet! I guess the diabetic foot will have to be another post. Keep checking back for Part 2 and I’ll keep your brain busy! I’m definitely not done yet!

How often do you teach patients how to use their glucometer? Tell me about it in the comments!

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Liu, Jx., Zhu, L., Li, Pj. et al. Effectiveness of high-intensity interval training on glycemic control and cardiorespiratory fitness in patients with type 2 diabetes: a systematic review and meta-analysis. Aging Clin Exp Res 31, 575–593 (2019).

Magalhães, J.P., Melo, X., Correia, I.R. et al. Effects of combined training with different intensities on vascular health in patients with type 2 diabetes: a 1-year randomized controlled trial. Cardiovasc Diabetol 18, 34 (2019).

Marcie Harris-Hayes, Mario Schootman, Jeffrey C. Schootman, and Mary K. Hastings. The Role of Physical Therapists in Fighting the Type 2 Diabetes Epidemic. Journal of Orthopaedic & Sports Physical Therapy 2020 50:1, 5-16

Mayo Clinic. (2020, May 13). Hypoglycemia.

Mayo Clinic. (2020, June 27). Hyperglycemia.

Centers for Disease Control and Preventions. (2021, April 28). Diabetes: Manage Blood Sugar.

The contents of this blog and all associated pages reflect the opinions of the author and should not be construed as medical advice. Please consult your doctor for medical advice.

Airway Clearance Techniques

Airway Clearance Techniques (ACTs) are the best practice for patients who are in acute exacerbation, sub-acute exacerbation or are stable with obstructive lung conditions.
Long-term management of obstructive lung disorders including cystic fibrosis, COPD, bronchiectasis, and chronic bronchitis, and those with impaired cough including ALS, SCI, and post lung transplant should include instruction in ACTs.

Pulmonary Hygiene takes a team – reinforce the regular performance of ACTs!

I have a special treat for you!

I created this a while back. All you MDTs out there will love it. This is a force progression (backed with evidence!) for applying, combining, and progressing airway clearance techniques. It starts out with the patient providing their own forces from the inside and outside, then adds the external forces you can apply as a part of your airway clearance techniques.

Brockway, K. (2017) Pulmonary hygiene toolbox – force progression tips
(Original content)

Tips for airway clearance techniques:

  • These are considered AGPs (Aerosol generating procedures)! Therefore, they require full PPE and an N95 mask per the CDC guidelines when performing with a patient with known or suspected COVID-19 (or any other viral infection of the lungs).
  • Always consider changing positions to utilize postural drainage positions to encourage increased secretion mobility.
  • When implementing oscillatory devices, keep in mind that not all oscillatory devices can be inverted or turned sideways and continue to function (such as the Aerobika). However, some can do this easily (like the Acapella).
  • Have tissues ready! My friends in ICU tend to use a cup. Secretion color and consistency matter and can tell you really important things!

Don’t forget about other tools in your toolbox!

  • Increase water intake: This thins secretions so they are more mobile.
  • Increase overall mobility: increasing mobility means increased respiratory rate and depth which naturally mobilizes secretions.
  • Change positions frequently: utilizing postural drainage positions or just changing positions frequently throughout the day reduces consolidation.
  • Utilize Mucolytics: for very thick secretions and/or patients who are not mobile to improve secretion consistency for better mobilization and expulsion.

So that’s just the intro! Come back often to find all kinds of great techniques and information to update your skills and get you ready to practice in the cardiopulmonary setting!

More from the Pulmonary Rehab Toolbox…

CO2 Retainers

Getting sciencey now! The science behind COPD and oxygen to help lead you right!


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Pulse Oximetry and O2 Saturation

This may seem simple… but it is my constant battle: valuable but so difficult.

This is one simple vitals measurement with one tiny tool. There can’t be that much to it…

Let’s go for a ride down the river.

The first day at your new job, there are lots of jobs for your team to do, but there just aren’t enough people showing up for the jobs. If these people don’t show up, you will still all get in your boats and go down the river to work, but there just won’t be enough people to get all the jobs done. You will work your butt off and feel exhausted, but the work just won’t get done.

The second day, all your team members finally showed up, but the boat company gave you fewer boats based on yesterday’s attendance. So now you have all the people to do the work, but you can’t get everyone down the river to work to do the jobs. Again, you will work so hard, be exhausted, and the jobs will not get done.

The third day, there is a storm. There are trees fallen across the river. You have your boats and people this time, but it is really difficult to get down the river to work because there are so many tress in the way and the path is very narrow. So the people who get there will work really hard, feel exhausted, and the jobs still won’t get done.

The fourth day, a new company moves in and builds a dam upstream. They will only let so much water flow through the dam and its just not enough to float your boats down the river, so you have to walk to work. You’ll get there, slowly, but you’ll lose a lot of time and you’ll be exhausted and the work won’t get done.

This is how our patients feel in different states of oxygen deficiency.

People = Oxygen Molecules
Boats = Hemoglobin
Trees = DVTs/atherosclerotic plaques/arterial calcification
The River = Cardiac Output

There is a whole set of considerations to using pulse oximetry. SpO2 only measures the saturation of oxygen in hemoglobin. But what if there isn’t enough hemoglobin? You can have them 100% saturated but still have a very breathless patient who need critical intervention (a transfusion!). And what if there isn’t enough cardiac output, literally not enough blood leaving the heart (aka Ejection Fraction) to go to the body? Now your patient doesn’t even have enough breath to walk to the bathroom and your oximeter is reading 100%. What if you have enough output, but the vessels are obstructed due to PVD or PAD or a DVT? Pulse oximeter still reads 100%, if you can get a reading at all.

The story of the people and their boats is how I explain each of these deficient states to my patients depending on what state they are in.


Yep. That’s how I feel about pulse oximetry. I NEED to know when my patient is desaturating. I need to know how much. I also need to know if they are too saturated! And, in the home environment, or in the gym at my SNF, I have pulse oximetry to give me those answers. The unfortunate thing about pulse oximetry is how unreliable it can be and how difficult it can be to use. But, like I said, I NEED it!

If you are regularly using a fingertip pulse oximeter, there are a more than a few things you need to know:

  • You need to simultaneously palpate or auscultate the patient’s heart rate/pulse rate during use. If the heart rate doesn’t at least somewhat match from manual palpation to the device reading, you cannot trust the oximetry reading.
    • These devices require a regular and relatively strong heart rate to provide a proper reading.
    • Most oximeters have a heart rhythm bar that goes up and down with each beat. If that bar is not going up and down in a regular fashion, the oximetry number is not correct.
  • If your patient has any cardiovascular comorbidities, odds of a pulse oximeter working are reduced. You may be thinking, “Well shoot, Doctor B, that’s who I need to be using this with.” And you’d be right.
    • Does your patient have A-Fib? Definitely won’t work. (see above)
    • Do they have PVD? Almost definitely won’t work. (see above)
    • Do they have peripheral neuropathy? Probably won’t work.
    • Do they have Raynaud’s Phenomenon? Probably won’t work.
    • Do they have essential tremor? Definitely won’t work.
  • If your patient has no fingers or toes, I don’t even know what else to tell you. There are different types of pulse oximeters that can be taped to different body parts like ears, feet, hands, arms, wherever you can get good contact. They are regularly used in NICU settings. But, I don’t carry one of those in my bag and my SNF doesn’t have one. So…
    • Unfortunately, these other devices come with their own flaws. Performing isometric contractions of the muscles where they are located can drain the local oxygen supply and show falsely depleted oxygen saturation. (Death gripping a walker handle will impair fingertip oximeter readings.)
    • They are also more prone to interference from body movement if you have to perform any other type of activity with the body part it is attached to.

So, what the heck do I do with this thing?

Correlate clinically.

Your pulse oximeter shows desaturation to 84% but your patient is happily talking and exercising with you without shortness of breath and they have no pulmonary pathology. Obviously a false reading.

However, your patient is sweating, panting, and slightly dusky around their mouth while walking with you. You know they recently had COVID-19. Your pulse oximeter says 96%. Obviously a false reading.

If things aren’t making sense, pick a different finger and make sure that finger is warm before putting the oximeter on it. If that doesn’t work, change your batteries.

That’s Troubleshooting 101, 102, 103, 401, and 700. Make sense?

Hint = SpO2 is oxygen saturation measured with an oximeter. PaO2 is the partial pressure of oxygen in the blood measured with an ABG.

image credit

So what’s normal?

Even debilitated patients who probably have a lower ejection fraction shouldn’t significantly desaturate with normal activity unless they have severe comorbidities, like end-stage COPD. If they are, they need supplemental oxygen to perform these tasks. A normal decrease in saturation with activity is 1-2% even if someone has been immobilized. SpO2 should be around 97-99% in healthy individuals.

However, if your patient desaturates more than 4%, or desaturates to less than 90% SpO2, with activity, this is a problem (unless they are a CO2 Retainer). If this happens, you should hopefully see some compensations in heart rate or blood pressure, or both, and it should recover with rest.

What if SpO2 doesn’t recover with rest?

If your patient’s SpO2 is dropping with basic household mobility, your patient is struggling to function, and their vitals show hypoxia, you either need to get them supplemental oxygen, or you need to titrate the supplemental oxygen they already have.

WHOA!!! Hold up, wait a minute!

I know, I know. You are thinking, “Oxygen is a drug, I can’t titrate it without a doctor’s order!” Yes, you are absolutely right. But are you going to let your patient go in to acute respiratory distress in the meantime? I think not.

While you are helping your patient recover from their desaturation with rest, breathing, and increased O2, get the doc (or their nurse) on the phone, let them know what you found and what you did. Ask them for some “titrate to” orders to help you out so you don’t have this problem anymore. I’m sure they will be happy to oblige you. Team work makes the dream work.

So what about COVID-19?

In the rush to open critical beds and move people out of the hospital as quickly as possible, rehab and nursing providers may not get the full opportunity to assess a patient’s response to activity, specifically their oxygen response. When you start seeing these patients in the post-acute settings, like home care, inpatient rehab, sub-acute rehab, or skilled nursing settings, you may find they weren’t quite ready to be off supplemental oxygen all together just yet. It is very possible your patients still may need supplemental oxygen with activity, even if they are well saturated at rest.

How do you know when a patient is orthostatic or just deconditioned as opposed to needing supplemental oxygen to prevent hypoxia with activity? The symptoms can be similar: shortness of breath, increased respiratory rate, fatigue, lightheadedness. So how do you know? Here’s how:

Take baseline vitals at rest (like really rest) in supine (HR/PR, BP, O2, RR)
Sit up and take another set of vitals
Perform an ADL or UE activity from seated and take another set of vitals
Stand up and take another set of vitals
Walk and take another set of vitals

If blood pressure drops, heart rate rises, and oxygen stays the same on the BOLD lines, you have orthostasis.
If blood pressure and heart rate elevate, and oxygen drops on the ITALICIZED lines, you have activity-induced hypoxia.

With orthostasis, blood pressure changes happen in response to changes in position with gravity. Blood pressure drops and the heart attempts to compensate by rising, but O2 saturation should stay the same, even in a deconditioned person. We will talk more details on this in another post.

With activity-induced hypoxia, blood pressure elevates and heart rate elevates in response to low oxygen levels (the body is trying to get more oxygen-rich blood out to the tissues to complete whatever work needs to be done), but the diffusion of oxygen across the alveolar membrane isn’t happening at a rate that can match the demand (problem with V/Q matching) due to the alveolar destruction caused by COVID-19 (or any other pulmonary pathology). This patient needs some supplemental oxygen. They could also benefit from some hyperinflation techniques if they have recently been ventilated, experienced pneumothorax, or any other condition that would result in collapsed alveolar clusters (aka restrictive conditions).

I get pretty high on my vitals soap box sometimes, but this is why. These numbers are where your decision making NEEDS to come from. You can’t base your treatment on how the patient looks or how they say they feel. You have to see the numbers for yourself and know the numbers are correct.

What’s next?

Start exercising! Left ventricular remodeling is important to get cardiac output up and helps to improve ejection fraction over time. Alternating intervals helps to alternate lung volumes which helps with reinflation of collapsed segments. These happen with exercise!

In the acute and immediate post-acute phase, you should be targeting a 5 on the Borg RPD scale (moderate) or whatever corresponds to moderate breathlessness on the scale you use. You don’t really want to go higher than that because of the severe pathology this patient is still fighting.

In the sub-acute and ongoing settings, start working them harder. If they begin to be more limited by deconditioning than breathlessness, switch to a Borg or Borg Category Ratio scale instead and target 7-8/10. Use heart rate calculations if you can (Call up your old college buddies, Tanaka and Karvonen) to be more precise in your prescription with 70-80% HRmax. Make sure you are utilized standardized measures to establish baseline function and demonstrate improvements over time!

Hey, Doctor B, I think you got a little carried away here…

Yea, probably. Thanks for sticking with me.

I will tell you that I’ve had all of these patients in the home and SNF settings. I’ve ordered supplemental oxygen at a home PT eval. I’ve explained a 15% ejection fraction and why this patient needed to wear oxygen even though his SpO2 was 97%. I’ve called the doc and requested a CBC to check hemoglobin levels (and I’ve been right). I’ve titrated oxygen for recovery and requested “titrate to” orders more times than I can count. I’ve read ABGs and found new CO2 retainers. If I’ve encountered it, you will, too. So I want you to be ready and understand what you need and why you need it.

That was a lot. If you want to know more, ask me in the comments!

More from the Pulmonary Rehab Toolbox…


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Hillegass, E. (2020). Vital Signs, oxygen, & exercise prescription: How are these impacted by COVID-19? PACER Project. Cardiovascular and Pulmonary sections of the APTA. Retrieved from

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 working with patients who are new to supplemental oxygen. This may be the case if you are working with someone who has had COVID-19 and is transitioning settings, or if you work with people who may be new to COPD or other lung diseases.

The first exacerbation of a chronic lung disease is always the scariest because the patient doesn’t know what to expect. They come home with all this new equipment and medicines, and they have no idea what to do with themselves. Usually, rehab and nursing can get them straightened out pretty quick, but sometimes you catch this on the fly and have to completely adapt your process.

Remember, for those who are new to oxygen, they may be pretty overwhelmed as it is. Taking in all this safety info and attempting to coordinate any changes to what they came home with will be very difficult for them as their cognitive load is already very high. Many of these things will fall to you to manage for the initial time frame. You’ll be lucky if they remember even half of what they were told as part of their discharge instructions.

Photo by Andrea Piacquadio on

So, on to the list of things we mentioned in the previous post on COPD management. I was going to go in to detail on these items in that post but decided it would just be too much and wasn’t necessarily specific to COPD management. These things can really be applied to all cases where supplemental O2 is required. This post is going to be specific to rehab considerations, but if you are looking for information on supplemental O2 delivery systems and devices, you can check out this post. These tips are all my own, and just what I’ve come to find works best in the long run.

Photo by cottonbro on

Are you ready for this? Here we go…

  1. Supplemental oxygen is typically delivered by a static concentrator that utilizes lengths of tubing that deliver oxygen to the patient wherever they are, which means tubing laying on the floor.
    • Tubing on the floor is a tripping hazard for the patient as well as any other people living in the home. This tripping hazard increases when the patient also uses an assistive device as this is one more (at least) point of contact with the floor that must be cleared with each step. The risks and benefits of utilizing this standard delivery method must be weighed and compensated for each patient individually. Here are some considerations:
      • How active is your patient?
      • Is your patient already a significant fall risk?
      • Are there others in the home that are a significant fall risk, for example, a spouse with dementia?
      • Does the patient utilize a wheelchair? Tubing on the floor creates a barrier and could be considered a restraint if the patient cannot wheel over the tubing in their chair.
      • Is there another option for oxygen delivery that would successfully meet the patient’s needs?
      • Is there another option for oxygen delivery that is within the payer scope?
    • And, yes, supplemental oxygen NEEDS to be worn in the shower. Showering takes a lot of energy and time which requires lots of oxygen. Without it, this particular ADL (and pretty much all ADL, if I’m being honest) are not safe.
    • Oxygen is flammable. Keep it away from gas stoves, lighters, cigarettes, and any other source of flame or high heat.
    • Don’t forget that, as a disease progresses, so too will the patient’s oxygen needs. They may require more or less depending on their disease.
      • If they have something chronic and long-term like COPD, they will probably require an increase over time. This is important to monitor closely as they could transition to being a CO2 retainer which would indicate some further work on your part, like reviewing ABGs and contacting the physician for a change in orders.
      • If they have an acute condition like pneumonia, they may be able to wean off of their oxygen over time. I’ve had this happen in patients, also. It’s a really great day when they get to send all that equipment back! But you’ll need to coordinate an overnight oxygen saturation study with the DME provider and perform a functional capacity test (like a 6-minute walk test) to be sure the patient is safe.
  2. Oxygen needs to be mobile to go with the patient when they go, and where a large static concentrator cannot follow. Therapists need to facilitate equipment setup to achieve this via mobile concentrators or other portable devices. This equipment must also be coordinated with their assistive device if they have one.
    • Mobile oxygen options vary by DME provider. You can have portable oxygen concentrators (or POCs), oxygen conservers, or cryogenic liquid oxygen delivery systems (Helio). All have their advantages and disadvantages and patients may have more than one delivery method depending on their needs.
    • Insurance will typically only cover one type of delivery system, and it is typically the standard concentrator with tubing if the patient is on standard flow orders. High flow orders can necessitate different delivery systems (such as liquid oxygen).
    • When used in conjunction with an assistive device, portable oxygen delivery systems can be attached in many ways.
      • Portable concentrators can go in a walker basket, on the walker seat, in a backpack, or over the shoulder in the carry bag.
      • Liquid oxygen has to be stored in an insulated bag (usually provided to the patient) and requires more equipment. The liquid has to be transformed in to a gas, which requires several steps, before it can be delivered to the patient. These tanks may require mounting brackets to the sides of wheelchairs, walkers, or the inside of the car to keep them safe. There are some that can be carried in carrying bags, but they are heavy (about 10 pounds) and require increased energy expenditure.
      • Small portable tanks with or without conservers (also known as “on demand” regulators) can be placed in a walker basket, carried in the carrying bag over the shoulder or on the walker handle, or can be mounted to a walker using a standard tank mounting bracket.
      • Mobile units will be limited in ability to provide adequate flow as most do not exceed 4 L/min, and will be limited in battery life based on flow needs. They will need to be charged whenever not in use.
    • When a patient is not regularly ambulatory, you may consider changing up their delivery system based on their functional status.
      • If they are in a recliner or bed most of the day with the exception of when you or another caregiver is present, you may consider have a spare small tank and canula to use for activity only, and have them use the concentrator at all other times.
      • If they are more mobile, you may switch them to smaller tanks to be used throughout the day and have them only use the concentrator at night for sleeping. This is a very successful approach in my practice. Patients love that they can be more mobile without tubing on the floor. Some concentrators come with an attachment that allows the concentrator to fill smaller oxygen tanks for exactly this purpose.
      • To make these changes, a physician order is not typically required as long as the flow rate isn’t changing. You can simply call the DME company, explain the safety concerns and ask for what you want.
  3. Backup oxygen supply is essential should there be an interruption in the power supply or the concentrator malfunctions.
    • All patients on supplemental oxygen should have a kilo tank, helio reservoir, or other backup supply available (maybe a charged portable concentrator) and know how to access it. Having the tank is great, but if their bedroom is upstairs and the tank is in the garage, that isn’t going to be helpful for them.
    • Kilo tanks have large regulators and can be used to fill smaller tanks or can be tapped directly via canula, but there needs to be at least 24 hours of spare oxygen in the home and the patient needs to know how to contact the DME company to let them know of a power supply failure so the DME can get more supply to them before their kilo runs out.
    • This is a step that is frequently missed in long term oxygen management, so remember to ask about it or check for a back up supply. If there isn’t one, call the DME company and get one delivered.
  4. Patients need to be educated on how to properly store tanks and swap regulators, as well as how to utilize their oxygen through any other delivery device such as their CPAP, a Duet, or a nebulizer.
    • Oxygen is still a drug that requires a physician order for proper use. It should not be used in any way other than how it is prescribed. However, it still remains our job to ensure it is used properly. Just like other drugs, patients can “ration” their supply if they are going to have to pay out of pocket for refills. This leads to hypoxia, cognitive impairments, and serious medical issues.
    • Spare tanks should be stored upright in some type of device that secures them from a fall. I have seen tanks chained to walls or inside of cars, I’ve seen velcro straps used, I’ve seen 2 liter pop bottle holder trays (they hold small tanks perfectly!). The DME company should have a solution for safe storage as part of their service to the patient. Backup supply tanks also need to be secured at they are tall and tipsy. Spare tanks should not be stored with regulators on them to prevent leaking.
    • Swapping regulators is an easy process, don’t be afraid that you are going to make the tank explode. There will be a loud puff of air but nothing more. Teach your patient to do this also.
    • If your patient is dependent upon supplemental oxygen, they also need to be utilizing this oxygen during other respiratory treatments. This includes CPAPs, BiPAPs, Nebulizers, Duets, and Acapellas.
      • CPAPs, BiPAPs, and nebulizers have a special attachment for supplemental oxygen to flow in. The DME providers should be setting this up, but sometimes it gets missed.
      • And if you are implementing a PEP device such as the Acapella or Duet, you need to make sure your patient is still getting their supplemental oxygen during use. Duets can run the oxygen directly through the bottom attachment. Acapellas allow the patient to still run oxygen via a nasal canula, but if that isn’t working, you can place the oxygen at the end of the Acapella so their are still breathing it in.
  5. Patients need to be educated on when to clean or replace canulas, tubing, masks, connectors, and any other parts of their oxygen delivery system to prevent pneumonia.
    • Canulas and masks should be replaced weekly, tubing biweekly or monthly (depending on the type of tubing). Connectors should be replaced with the parts they are attached to. So, connectors between lengths of tubing should be thrown out with the tubing. Tubing lengths should not exceed 50ft to maintain the proper flow rate.
    • Masks can be cleaned (just like CPAP masks) using vinegar and water, air dry. Tubing shouldn’t be cleaned as it retains too much moisture and can actually increase the risk of pneumonia. If you see moisture in the tubing, run the oxygen through it without having it attached to the patient until it is dry. (Put the patient on another source of oxygen while you do this.)
    • Dirty parts can lead to pneumonia and other respiratory infections. I’ve found that patients tend to have a drawer or box somewhere with all their “spare” tubing and canulas, not realizing that they are supposed to replace this stuff regularly.
    • If tubing or canula pieces become stiff (like from age or body oils), they should be replaced.
  6. Adaptations are available to make supplemental oxygen delivery more comfortable for the patient.
    • The most common one is a humidifier. It looks like a small cup of water attached to the concentrator. The oxygen creates bubbles in the cup if it is working properly. These typically require distilled water which leads patients to not refill them when they should, and then they don’t get used. They really do make that oxygen much more comfortable and humidifiers also prevent bloody noses and sore throats.
    • Ear padding is available for people who need to wear canulas and glasses or for people who have discomfort on their ears from the canula. I’ve even seen pressure ulcers on ears due to canulas so this is a big concern. The padding is easy to place on the canula, you just have to ask for it.
    • Canula face padding is also available for noses and cheeks to make the canula as comfortable as possible.

And the final tip I have for you about the management of supplemental oxygen is this: Watch your patient change from mobile oxygen to concentrator oxygen and back.

I do this with literally every patient I evaluate that uses oxygen, new or not. I will tell you that in seven years of doing home health care, I’ve only ever had two patients do this properly. I actually time them. No joke. I time how long it takes them to do it. I once timed a patient as they went three and a half minutes without oxygen while they were trying to figure out how to change from static to mobile oxygen sources. They were exhausted, short of breath (go figure), and desaturated to 84%. I intentionally let them go all the way until they were done, under my close supervision.

The most common mistake patients make is they don’t set up their mobile before taking off the canula from the concentrator. It usually goes down like this:

  1. I ask them to show me how they switch from concentrator to mobile tank
  2. They take off the canula for their concentrator
  3. They hunt around the house for their mobile tank
  4. They hunt around for a canula
  5. They get everything put together
  6. They try to figure out how to turn the regulator on (if there is even a regulator on the tank at all)
  7. They can’t see the numbers on the regulator so they have to get glasses…

Do you see where I’m going? They spend way too much time without oxygen trying to figure this out. That is why I always ask them to show me how they do it. By moving step 2 in the above process to the last step, they maintain their safety. One simple change, that’s all it takes. Most of the time, when I show people this, they are in awe. It’s like I waved my magic wand.

Now that I’ve rambled on and on about this, I need you all to go out and wave your magic wands. Go make those patients so much safer. Take the reigns of their oxygen management for a time to make sure they are safe and then teach them how to do the same.

Try out a few of these clinical pearls and let me know how it goes 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…”

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”


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Hardavella, G., Karampinis, I., Frille, A., Sreter, K., & Rousalova, I. (2019). Oxygen devices and delivery systems. Breathe (Sheffield, England)15(3), e108–e116.

Hillegass, E. (2020). Vital Signs, oxygen, & exercise prescription: How are these impacted by COVID-19? PACER Project. Cardiovascular and Pulmonary sections of the APTA. Retrieved from

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CO2 Retainers

Getting a little sciencey…

So I’ve been talking about a lot of different techniques for increasing inflation, ventilation, and (ultimately) perfusion that therapists can utilize with patients. However, I’ve been mentioning here and there that some of these need to be utilized with caution in patients who have obstructive lung conditions. Please heed my warning. Here’s one of the reasons why…

What is Hypercapnia?

Hypercapnia, also known as hypercarbia and CO₂ retention, is a condition of abnormally elevated carbon dioxide levels in the blood. PaCO2 > 45 mmHg.

What this basically results in physiologically is that the normal respiratory drive no longer exists. The changes in PaCO2 that the body experiences over the long term destroy certain receptors, so the only force keeping a CO2 retainer breathing is a lower O2 saturation. Titrating someone who is a retainer to above 95% can actually STOP them from breathing! Their body realizes a lack of NEED for oxygen.

What causes Hypercapnia?

  • COPD (chronic bronchitis + emphysema)
  • Interstitial lung disease
  • Hypoventilation
  • Narcotic overdose
  • Obesity
  • Obstructive Sleep Apnea (OSA)

Symptoms of hypercapnia

What Can You Do?

  • Obtain “titrate to” oxygen orders for a tailored approach to maintaining resting and active saturation between 88-92% (or whatever other parameters the pulmonologist decides upon) to reduce risk of hypoxemia but also manage hypercapnia.
  • Refer the patient for Sleep Study if they have a history of Acute Hypoxic Respiratory Failure
  • Encourage the use of CPAP/BiPAP (Non-Invasive Ventilation (NIV) treatment)

Did you know?

Daytime hypercapnia and nocturnal hypoxia are predictors of CPAP failure in patients with OSA-COPD overlap syndrome. An increase of CT90% (defined as the time with SpO2 < 90% of total sleep time) by 1% increases the likelihood of CPAP failure by ∼6%.

Bilevel positive airway pressure (BiPAP) therapy effectively alleviates hypercapnia in patients with primary CPAP failure.

What about COVID-19?

BiPAPs have been found to not be effective for the treatment of patients with COVID-19 (WCPT, 2020 – see resources page). However, NIPPV has been utilized in certain circumstances which is a similar intervention that uses a CPAP or BiPAP machine. High Flow Nasal Oxygen (HFNO) has also been utilized due to the severe desaturation COVID patients experience. We will talk more about these in another post.

This becomes a risk vs benefit analysis. If you are seeing a patient who has COPD and is or is not a CO2 Retainer, but you feel they may need some of these inspiratory or hyperinflation interventions, then provide them. But do so knowing that you should be monitoring oxygen levels, limiting hyperinflation as much as possible to obstructed segments, and know the signs and symptoms of decline in your patient.

As we’ve discussed in other posts, patients who have COPD are at particular risk of decline when also affected by COVID-19 because of their long-term use of corticosteroids. When they return home or if they are being treated in the home primarily, you may end up treating a COPD exacerbation more than the effects of COVID-19. It will be patient-dependent. Keep your AGP precautions in mind.

As PTs and other rehab professionals, we cannot diagnose someone as a CO2 retainer, but we can definitely look at the ABGs and find our answers. Have you had any difficulty obtaining altered orders or parameters for patients who are CO2 Retainers? Let me know your stories in the comments!

More from the Pulmonary Rehab 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”

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”


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”

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The Basics of Lung Auscultation

If you are going to be providing pulmonary interventions, you should probably have a strong idea of how to auscultate the lungs. The importance of this is pretty paramount. You have to know WHAT you are listening for and you have to know HOW to listen. There are a lot of variables when it comes to disease state, but if you have a stethoscope, just start listening to all your family members to get an idea of what “normal” sounds like.

The method of performing auscultation that gives you the most information is to use the “S” pattern. This includes listening from top to bottom and left to right with the ability to compare right and left sides of the same lung segment. You also MUST listen to both the front and back of the lungs to ensure you are getting all the segments. If you don’t, you may miss the left lingular segments which is where stuff likes to hide.

So let’s start with the basic anatomy refresher. We aren’t going to spent too much time here. What is most important is that you listen to all segments and compare sides.

image source

When auscultating, you want to start in the same place every time, typically the patient’s right upper lobe, then traveling across the sternum to the left upper lobe, then inferiorly, and then across. This is what creates the “S” pattern.

image source

Moving On…

The How To:

Listen at each point for two full breaths. Keep in mind that WHAT you hear depends on what depth of breath is being taken. Shallow breaths don’t move air in the bases of the lungs so you don’t typically hear sounds there! However, hearing NOTHING is also a problem! If you don’t hear anything, here’s what to do:

  • Check your stethoscope! Some have heads that swivel to channel sound toward different sides (bell vs. diaphragm). If the head got turned, you won’t hear anything.
  • Look down. This helps reposition the ear pieces to channel the sound directly in to your ears. You can also lift the ear pieces upward, same effect.
  • Ask your patient to take a deeper breath.
  • Listen longer. A typical respiratory rate is 12-16 breaths per minute. This is one breath about every 4 seconds. If your patient is bradypnic, you may have to wait longer.

What Should You Hear?

Normal lung sounds (named “vesicular” sounds when auscultated over the peripheral segments) should be somewhat quiet, but sounds that are too quiet are what we term “diminished.” It can be typical to hear diminished sounds in a patient who is obese or who doesn’t utilize much lung volume. If they are not utilizing much lung volume, this is a great opportunity for you to intervene with some diaphragmatic breath training and/or IMT use for diaphragm strengthening!


Other normal sounds include bronchial (which are only normal when auscultated over the bronchials) and bronchovesicular (which are only normal when auscultated over the bronchioles).



It is important to remember that a normal sound that is auscultated in a place not considered to be normal is an adventitious sound.

Adventitious Sounds

An advantage for you, not for your patient… Adventitious sounds can be used to determine what pathology is present and what treatment needs to be performed.

Crackles (also known as “Discontinuous sounds”) can be heard over the peripheral airways also. Crackles can be a sign of COPD, bronchitis, CHF, Pneumonia, or atelectasis depending on when they happen in the breath cycle. Crackles can be fine (like bubbles gently popping) or course (like tearing Velcro apart). These sounds should tell you that you need to perform some interventions. ACBT helps with this.


Stridor is going to be a very important sound to know when assessing or treating patients with COVID-19. Stridor is typically associated with upper airway narrowing. However, it may also be present in extubated patients who come home after being hospitalized. If stridor is just beginning, your patient may need some urgent medical intervention. Hopefully, they will be moving toward the end of it.

Early Stridor

Rhonchi (also known as “low pitched continuous sounds”) are what I’ve always termed “the goose honk”. Rhonchi are heard when large amounts of mucus are present in the larger airways. These types of sounds are good indicators that some pulmonary hygiene is needed. ACBT is really useful here, as well as FETs or a PEP if your patient is too weak to perform FETs well. And sometimes you just need a good cough. If this patient has a trach, they will need suction.


Wheezes (also known as “high pitched continuous sounds”) are a fairly common adventitious sound that many people have heard. There are several tones and types, but overall, they indicate airway obstruction of some degree. You need to intervene here with some pulmonary hygiene interventions. ACBT is particularly useful here because wheezes can be in the smaller airways which can be targeted with ACBT. Segmental breathing may also be helpful if you can pinpoint the segment through your auscultation. PEP may also be useful.


Absent lung sounds can mean serious issues. If you have already tried the above techniques to modify what you hear and have had no luck, and your patient appears to be struggling, they may be experiencing a pneumothorax or severe atelectasis and you are auscultating right over it. There could also be something other than lung tissues present. If there is a tumor or other object that does not perform gas exchange in that particular location, you won’t hear air movement.

Please also check your patient’s medical history. If you are experiencing absent sounds, your patient may have had a lobectomy and there is no lung tissue present where you are auscultating.

If you happen to hear gargling sounds, you are auscultating too far inferiorly and have hit a digestive organ!

I also auscultate AFTER performing interventions and like to document the secretion movement (because you may hear it somewhere else after interventions) or the lack of adventitious sounds along with improved patient presentation indicating that secretions are no longer impairing ventilation!

BONUS!!! I found this video specific to adventitious sounds present in patients with COVID-19. You’ll hear the combination of several of the sounds you just listened to!


Now get to listening! Remember, you have to know what normal sounds like, so make sure you are listening to as many lungs as you can!

Comment below to tell me about a crazy sound you’ve heard while performing lung auscultation!

More from the Pulmonary Rehab Toolbox…


HFNO stands for High Flow Nasal Oxygen. This is something that was used frequently in patients who were desaturating quickly with symptoms of COVID-19. It has the ability, through the use of several different devices or setups, to deliver very high concentrations of supplemental oxygen to patients with advanced pulmonary diseases or conditions. In theContinue reading “HFNO”


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Follow @DoctorBthePT on Twitter for regular updates!

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 by several things such as genetic diseases (alpha-1-antitrypsin deficiency, for example, which causes emphysema in children and adults), lifestyle choices (such as smoking), work environments with poor engineering controls and toxic output (asbestos, coal, and steel production), or community/home environments that require regular burning of substances with toxic output for a heat source or for food preparation.

Like the name suggests, it is an obstructive lung condition, meaning that stuff gets in the airway making it hard for air to get OUT of the lungs. Air trapping, mucus hypersecretion, physiological and physical changes to the body, chronic cough, and decreased overall activity level are all signature components of COPD. COPD used to be ranked based on severity for GOLD levels which are based on FEV1. This system is not part of a clinical picture of symptoms assessment instead of the sole descriptor:

GOLD, 2020

COPD is often accompanied by (or even caused by) other chronic diseases such as left heart failure. It can exist in isolation, but even then, the treatments tend to induce other chronic conditions. Long term COPD management with corticosteroids has a host of side effects including osteoporosis, diabetes, vision impairments, and increased risk of infection (among others). Long term use of bronchodilators (inhalant medications, typically) have been linked to myocardial infarctions, hypokalemia, and bronchospasm. These side effects lead to some interventions being contraindicated (such as percussion) that would otherwise be helpful in COPD symptom management.

If you treat patients with COPD regularly, you tend to get a feeling for what COPD looks like. That’s because it comes with physiologic changes that eventually result in physical changes (similar to most chronic diseases!) that can be spotted across the room: barrel chests, blue-ish lips, digital clubbing, sunken eyes, coughing regularly, accessory musculature popping out of the collar of a shirt… And those are just the things we can see. The thinks we can’t see are worse. Chronic cough is also associated with urinary incontinence and chronic back pain, and diseases of breathing are associated with depression and anxiety.

Our goal with patients who have COPD is two-fold:
Reduce the risk of rehospitalization and improve quality of life.
These two goals include all the medical management and functional interventions we would apply. But first…

We have to quantify it

Just because someone has COPD doesn’t mean they necessarily need a PT or any other rehab provider involved in their care, so we need to make it clear when and why we are necessary. We need to express what deficits they are facing because of their COPD (or any other comorbidity). You’ll need some tools for this. There are many that are somewhat generic, but there are some disease specific tools, too. These tools are great because they can really help direct your interventions to give the patient the most BANG for their BUCK! We will talk about a few of them here, but there are many.

The COPD Assessment TEST (CAT) – highly recommended and free, this is the test recommended by the Global Initiative for Chronic Obstructive Lung Disease (GOLD)

Leicester Cough Questionnaire (LCQ) – Used frequently in research specific to COPD

Chronic Respiratory Questionnaire (CRQ) – proprietary assessment owned by McMaster University

SF-36 – More generic but a wealth of evidence to support its applicability (developed at RAND as part of the Medical Outcomes Study)

The Cough and Sputum Assessment Questionnaire (CASA-Q) – also proprietary, but validated with the SF-36 and disease specific

The Patient Reported Outcomes Measure Information System (PROMIS) Global Rating Scale – a free NIH funded HRQoL Questionnaire

Many physical function and exercise capacity tests can also be utilized, such as the 6-minute walk test, the 2-minute step test, the 400 meter walk test, and many others. For more information on standardized tests and measures that are valid for patients with COPD, check out SRALab (formerly I like to use a combination of different measures to better capture the “whole-patient” picture, one physical, one subjective report, and maybe one or two others based on the reported deficits.

Then we have to treat it

You may find several areas of impairment based on your chosen outcomes measures, so you may have several areas of physical, mental, and emotional function to address, either by yourself or in conjunction with your team. Chronic diseases like COPD, which deplete oxygen supply to the brain and weigh a heavy burden on patients and their caregivers, tend to have long lasting emotional and mental effects, so don’t forget to refer to your colleagues across disciplines.

For people with COPD, secretion management is also going to be a large part of their long term plan, but it is also something they face acutely in the hospital or subacute setting that rehab therapists can very easily improve. We know that, independent of any other factors, mucus hypersecretion is a risk factor for hospitalization and death. So what do we have in our toolbox? Oh, so many great things! Click the links for more details of each tool or technique.

AcapellaTM Oscillatory PEP Devices

Oscillatory PEP therapy is effective at increasing secretion transport, decreasing breathlessness, reduced hyperinflation, and is as effective as other airway clearance techniques at improving disease-specific quality of life. However, flutter valves have ben found to be more fatiguing for patients than other types of airway clearance such as the active cycle of breathing (ACBT). Patients with COPD do not experience greater discomfort when performing one airway clearance technique over the other, even when utilizing gravity-assisted positions (or postural drainage). ACBT and oscillatory PEP have near equal outcomes for patients with COPD when performed with or without postural drainage positions when it comes to dyspnea, cough frequency, and overall weakness. Although, ACBT was found to be more efficient as moving secretions from the smaller focal airways than oscillatory PEP interventions. There were also no differences in the effects on lung function as both tools improved FEV1 and FVC. In my mind, that’s great news!

That means we can utilize either one, depending on our goals with the patient, and still achieve similar outcomes! If our patient fatigues easily, we may stick to the ACBT, but if we are targetting dynamic hyperinflation or need to significantly improve overall quality of life we may chose a PEP. In my regular practice, I give both and here’s why:

  • PEP devices are easier to use, remember to use, and take less time to perform than the ACBT.
  • Having a PEP around provides a visual reminder that the patient needs to do airway clearance techniques
  • I want the effects of both when I treat patients with COPD, as many patients need to improve their disease-specific quality of life and their dynamic hyperinflation, but also fatigue quickly, and I want them to have options. Having options for long term management that can all be performed independently with or without devices increases the chance they will actually be used.

No technique for airway clearance is as effective on its own as it is when combined with something else. Postural drainage can be combined with most techniques to target specific segments.

Then we have to manage it

In addition to secretion management, patients with COPD tend to need supplemental oxygen. There is a high degree of training that is required for the effective use of this drug including how to manage the equipment, how to therapeutically manage the drug from a rehabilitation perspective, and how to incorporate the equipment and the drug in to everyday life. There are many safety concerns that accompany supplemental oxygen delivery, which are usually the reasons rehabilitation providers are brought in. However, if we can prevent the safety events from happening at all by seeing the patient earlier, rather than later, that’s all the better. You can click the links for more information on each piece of this, but I’ll address some of the safety concerns in brief:

  • Supplemental oxygen is typically delivered by a static concentrator that utilizes lengths of tubing the deliver oxygen to the patient wherever they are, which means tubing laying on the floor.
  • Oxygen needs to be mobile to go with the patient when they go where a large static concentrator cannot follow. Therapists need to facilitate equipment setup to achieve this via mobile concentrators or other portable devices. This equipment must also be coordinated with their assistive device if they have one.
  • Backup oxygen supply is essential should there be an interruption in the power supply or the concentrator malfunctions. All patients on supplemental oxygen should have a kilo tank or other backup supply available and know how to access it.
  • Patients need to be educated on how to properly store tanks and swap regulators, as well as how to utilize their oxygen through any other delivery device such as their CPAP, a Duet, or a nebulizer.
  • Patients need to be educated on when to clean or replace canulas, tubing, masks, connectors, and any other parts of their oxygen delivery system to prevent pneumonia.

I could really just keep going on this forever… I’ve spent a large amount of time teaching patients how to properly use, manage, and maintain their supplemental oxygen. Maybe I’ll just do a whole other post on factors to consider when managing supplemental oxygen. Keep your eyes peeled for that!

Also, keep in mind the long term changes that happen over time with COPD. We need to be keeping our eyes on those ABGs and looking for an elevated PaCO2 which might tell us that our patient has become a CO2 retainer. This is critical in the management of our patients with COPD and will inform how you manage and monitor their oxygen. Click the link to read more. We may also need to strongly promote fall prevention strategies as these patients have a high risk of falls and a high risk of injury with falls. We will talk a little bit more about this later.

Speaking of long term changes, even though we’ve talked this whole time about getting all that trapped air out, we need to briefly talk about getting air in. Specifically, long term diaphragm weakness is to be expected with physical changes like becoming barrel chested. Diaphragm strengthening using an IMT is crucial, but to be used with caution.

Finally, we need to exercise them!

Finally, right? I bet you thought this part would never come. There is currently no Clinical Practice Guideline for Physical Therapists in the Management of COPD (I checked, twice, and emailed people), but the evidence for high-intensity interval training (HIIT) is pretty clear.

High-intensity interval training produces significant increases in maximal exercise capacity based on outcomes of the 6 minute walk test, as well as a reduction in lower extremity discomfort during exercise, which may be due to peripheral muscle changes in response to exercise. Patients with COPD who perform high-intensity interval training respond with an improvement in VO2max that is two to three times greater than with typical moderate intensity training. High-intensity interval training is also known to produce physiological changes including left ventricular remodeling that improves the overall patient response to exercise with increased oxygenated blood traveling to the muscles and other tissues. HIIT also produces improvement in functional activity and exercise capacity (measured via the 6 minute walk test), improvement in lung function (such as FVC), and in work efficiency.

The overall consensus on HIIT for patients with COPD is that, in the end, the outcomes are the same as when using moderate intensity continuous exercise, however, the results are achieved much faster and patient compliance is higher. So High-Intensity Interval Training is how you give your patients more BANG for their BUCK.

If you are not a provider in a pulmonary rehab setting, do NOT forget about pulmonary rehab! Evidence has shown that pulmonary rehab programs result in 52% fewer hospital readmissions, 4.27 less days in the hospital, and 19% fewer deaths in the same time frame in comparison to patients with COPD who did not have pulmonary rehab!

Photo by Burak K on

Of course, HIIT, if designed properly, can be performed by almost any patient at any level. I can absolutely make a HIIT program out of breathing exercises. I’ve done it. So if you have no arms and legs, I can give you a HIIT program. But this cannot be done alone. Address those functional deficits, retrain breathing patterns, improve ADL performance efficiency, and ensure oxygen safety. Manage the medications and their side effects, monitor the oxygen and exertion levels, and instill confidence that COPD may be life-altering, but it doesn’t have to be life-ending.

With chronic disease, it’s a package deal.

What specialty referrals do you make for your patients with COPD? Tell me about them in the comments!

More from the Pulmonary Rehab Toolbox…

The Counting Talk Test

Time to give you guys another tool. This one is especially important for patients with COVID-19, and it’s not terribly often that we get an objective measure for exertion. I’ve found the counting talk test to be critical in quantifying exertion in my patients with respiratory diagnoses. This measure is phenomenal for taking breathlessness inContinue reading “The Counting Talk Test”


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Adolfo, J. R., Dhein, W., & Sbruzzi, G. (2019). Intensity of physical exercise and its effect on functional capacity in COPD: systematic review and meta-analysis. Jornal Brasileiro de Pneumologia45(6), e20180011. Epub September 26, 2019.

Birring SS, Prudon B, Carr AJ, et alDevelopment of a symptom specific health status measure for patients with chronic cough: Leicester Cough Questionnaire (LCQ)Thorax 2003;58:339-343.

Chakravorty, I., Chahal, K., & Austin, G. (2011). A pilot study of the impact of high-frequency chest wall oscillation in chronic obstructive pulmonary disease patients with mucus hypersecretion. International journal of chronic obstructive pulmonary disease6, 693–699.

D’Abrosca, F., Garabelli, B., Savio, G., Barison, A., Appendini, L., Oliveira, L., Baiardi, P., & Balbi, B. (2017). Comparing airways clearance techniques in chronic obstructive pulmonary disease and bronchiectasis: positive expiratory pressure or temporary positive expiratory pressure? A retrospective study. Brazilian journal of physical therapy21(1), 15–23.

Global Initiative for Chronic Obstructive Lung Disease (GOLD) (2020). Global Strategy for the Diagnosis, Management, and Prevention of COPD – 2018 Report. [Adobe Acrobat document]. Available from:

Katajisto, M., & Laitinen, T. (2017). Estimating the effectiveness of pulmonary rehabilitation for COPD exacerbations: reduction of hospital inpatient days during the following year. International journal of chronic obstructive pulmonary disease12, 2763–2769.

Lee, A. L., Burge, A. T., & Holland, A. E. (2017). Positive expiratory pressure therapy versus other airway clearance techniques for bronchiectasis. The Cochrane database of systematic reviews9(9), CD011699.

O’Donnell A. E. (2018). Medical management of bronchiectasis. Journal of thoracic disease10(Suppl 28), S3428–S3435.

Rand Healthcare. (2020). The 36-Item Short Form Survey. Retrieved from

Ries, A. L., Bauldoff, G. S., Carlin, B. W., Casaburi, R., Emery, C. F., Mahler, D. A., Make, B., Rochester, C. L., Zuwallack, R., & Herrerias, C. (2007). Pulmonary Rehabilitation: Joint ACCP/AACVPR Evidence-Based Clinical Practice Guidelines. Chest131(5 Suppl), 4S–42S.

Ross, L. M., Porter, R. R., & Durstine, J. L. (2016). High-intensity interval training (HIIT) for patients with chronic diseases. Journal of Sport and Health Science. 5(2):139-144. Retrieved from

Ryrsø, C.K., Godtfredsen, N.S., Kofod, L.M. et al. (2018). Lower mortality after early supervised pulmonary rehabilitation following COPD-exacerbations: a systematic review and meta-analysis. BMC Pulm Med18,154.

Shen, Y., Huang, S., Kang, J., Lin, J., Lai, K., Sun, Y., Xiao, W., Yang, L., Yao, W., Cai, S., Huang, K., & Wen, F. (2018). Management of airway mucus hypersecretion in chronic airway inflammatory disease: Chinese expert consensus (English edition). International journal of chronic obstructive pulmonary disease13, 399–407.

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The (Very) Basics of Heart Auscultation

I was seeing a younger man in the home setting after a CABG x3 procedure. When I evaluated him, I was a bit frustrated because he had impaired cognition and had significant comorbidities for a younger man, none of which was in his referral information. Instead, I had the pleasure of just picking up on these things as I went along through my evaluation. His caregiver was reporting to me that he was very fatigued, very confused, very not himself since the surgery. He was a smaller man and did not seem to be exhibiting any signs of fluid overload. So I went on to what I typically look for in a patient immediately after CABG: orthostasis. In my article about Beta Blockers, we discussed how these medications are typically prescribed along with other medications after CABG procedures and this frequently results in orthostasis.

I began to perform the standard four-position orthostatic assessment that I mentioned in those posts and found him to be significantly orthostatic, to the point where I could not stand him up for more than a few seconds before he just sat down on his own due to being “lightheaded”. This seemed a bit extreme, but he was also likely dehydrated. However, yellow flags were going up in my head. I decided to investigate further. I noticed when taking his pulse and blood pressure that his heart rhythm was irregular so I took an extra listen to the main equipment.

La – Da – Da – La – Dub… Uh Oh.

This man’s heart sounded like an engine misfiring on all cylinders. There was some serious electrical disturbance going on here. I could hardly make sense of the sounds I was hearing. I contacted the cardiologist’s office and reported my findings (which probably sounded like I was completely unable to auscultate heart sounds… “uh, your patient’s heart isn’t demonstrating a typical contraction pattern upon auscultation…” was the best I could do without sounding just foolish).

Thankfully, his primary nurse arrived shortly after I discovered these findings and we had the opportunity to talk it over and attempt to figure it out. Ultimately, we decided he needed to go in and he was admitted.

So let’s take a look at heart auscultation. There are two main methods to do this, but, for the sake of simplicity, I’m just going to discuss this one. The “All Physical Therapists Move” method (also known as the “All Physicians Take Money” method) is the easiest to remember what you are actually listening to.

All. A is for Aortic Valve. Auscultating this structure will need to be done over the right second intercostal space at the sternal border. This is your “Dub”.

Physical. P is for Pulmonic Valve. Auscultating this structure will require you to place your stethoscope at the left second intercostal space, also at the sternal border. This is also your “Dub”.

Therapists. T is for Tricuspid. To auscultate this structure, place you stethoscope in the left fifth intercostal space, just lateral of the sternal border. This is your “Lub”.

Move. M is for Mitral (Also known as Bicuspid). To auscultate this structure, place your stethoscope in the left fifth intercostal space at midclavicular line. HOWEVER, this can be difficult to do with some female patients, and auscultation of sound may be difficult if the patient exhibits a bariatric build. So it can be easier to auscultate this valve at the same level, but at the midaxillary line. I typically perform this auscultation in this manner. This is also your “Lub”.

Next you need to know what you are listening for. There are four common heart sounds: S1, S2, S3, and S4. You really only want to hear two of them (S1 & S2), but sometimes you get a third or fourth thrown in. This can mean absolutely nothing, or it can mean poor cardiac function. It depends on the patient.

S1. “Lub” This is the normal sound of the Mitral and Tricuspid valves closing.

S2. “Dub” This is the normal sound of the Aortic and Pulmonic valves closing.

S3. An abnormal sound heard shortly after S2. It typically indicates delayed ventricular filling. This can indicate heart failure in some patients.

S4. Another abnormal heart sound heard shortly before S1. This sound tends to be more problematic as it indicates significantly delayed ventricular filling. This sound is regular associated with coronary artery disease, aortic stenosis, hypertension, or a heart attack.

***HOWEVER, in athletes, an S4 can be normal as it can indicate very efficient cardiac function or physical changes to the heart structure due to training (known as Athlete’s Heart). It is important to distinguish between this and serious clinical pathology. Athlete’s heart is a particular collage of findings including systolic murmur, S4 gallop sounds, and bradycardia in an asymptomatic and well-trained patient. Up to 1/3 of athletes have various electrical rhythm anomalies, some that occur only during exercise, and this can be completely normal. However, symptoms can be similar to hypertrophic cardiomyopathy so cardiac workup is warranted. Typically only an ECG is needed.***

So what are these sounds telling us? The closing of these valves is in precise timing, only about 0.1 second between S1 and S2. So if we are hearing other sounds, the timing is off. Similar to a car engine, this means bad things are probably coming. Extra sounds indicate electrical anomalies that can be seen on EKGs. So what does normal electrical heart function look like?

The usual path looks like this:

Sinoatrial (SA) Node –> Atrioventricular (AV) Node –> Bundle of His –> Atrioventricular (AV) Bundle –> Purkinje Fibers

But many different things can throw a wrench in to this system. In my post on beta blockers, I talked about atrial fibrillation which is just one of the many rhythm disorders we can see. I’m not going to pretend to know more about the electrical function of the heart than a cardiac nurse, so I’m going to let him give you this really awesome explanation. He also goes in to the easy way to read and interpret EKGs. His description makes this so easy to understand so I highly recommend watching it!


As a rehab clinician who is working in most settings, you don’t have to know ALL the details. What you do need to know is what is normal. That way, when you come across something abnormal, you can identify it and make sure it is addressed by the appropriate person. So, just like I recommend when it comes to lung auscultation, just start listening to everyone’s heart! Patients don’t know the different between listening to their heart and listening to their lungs so just listen to it all while you are there. Get an understanding of the variations on normal and try out different auscultation spots like I mentioned above. Soon, you’ll be identifying abnormal sounds and maybe even saving a life by early detection. You’ve got the skills!

Have you ever heard a crazy set of heart sounds? Or listened to heart sounds on something other than a human? Tell be about it in the comments!

More from the Pulmonary Rehab Toolbox…


“Whoops! Down I go! I thought I was going up, but apparently not!” I have heard this many times. Sometimes I hear it from the people around me just generally throughout the day. They black out or see stars or feel “whoozy” or report being lightheaded when they stand up from the couch or getContinue reading “Orthostasis”

The Beta Blockade

Ugh, medications… I know, I know. I will try to make this as painless as possible. This one matters. It REALLY matters. For patients who have COVID-19 and for patients who don’t. Please take a quick read. Let’s start off by asking some questions. What does a β-blocker do? Blocks norepinephrine and epinephrine from bindingContinue reading “The Beta Blockade”


We have been hearing all kinds of things about proning. What’s the big deal? Aren’t we just flipping people over? Well… yes! That’s exactly what we are doing. But here’s why its a bit more complicated than that. We’ve already talked about the role of PTs in supporting and improving V/Q matching. Proning helps withContinue reading “Proning”


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Magic In Nursing Team. (2017). EKG/ECG Interpretation (Basic): Easy and Simple!. Retrieved from

McKelvie, R. (2019). Athlete’s Heart. Merck Manual: Professional Version. Retrieved from on 6/22/20.

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Rule of 2’s

So today, we are going to focus on the role PTs and PTAs need to be filling in the treatment and management of congestive heart failure. The first thing you need to address is the rule of twos. Don’t assume someone else had ever educated your patient about this. I cannot tell you how many patients I have seen on their 3rd or 4th exacerbation who have never been educated on fluid restrictions or daily weights (FYI, its all of them).

Obviously there are different stages of heart failure and the patients you are seeing may not be as advanced as some of the patients I am seeing, but that doesn’t mean they don’t need to be managing their condition. The different stages of heart failure all have different needs, no let’s take a look:

Stage A: Pre-Heart Failure. This basically means that the patient is at higher risk of developing heart failure, but they aren’t quite there yet. They probably already have CAD, CKD, DM, HTN or some other set of comorbidities that is leading them down this path. Probably starting some beta blockers and/or ACE inhibitors here. This is the stage we HOPE to see them in because exercise can make a huge different here!

Stage B: Heart Failure. This is the real deal. Cardiac dysfunction is starting to show its ugly face here. Beta blockers and ACE inhibitors continue, and there will likely be a few other medications added like spironolactone or a different kind of diuretic like hydrochlorothiazide (HCTZ). All of these have some nasty side effects. Patients may start showing a reduced ejection fraction if they have HFrEF (reduced ejection fraction). Cardiac valve repairs/replacements and coronary stenting are common here. The disease manifests here as structural changes to the heart. Of note, HIIT style-exercise has shown significant evidence for promoting left ventricular remodeling in an effort to stop or reverse this process! Intensities up in the 90-95% HRmax range are necessary.

Stage C: Heart Failure with active symptoms. These patients tend to show the symptoms regularly, and have now experienced significant changes to their heart morphology. Shortness of breath is common along with fatigue, edema, and nocturia. This is the stage at which we start implementing the Rule of 2s. Pacemakers and/or ICDs make their appearance here if rhythm drugs fail. These are the patients I see often and I still have them doing HIIT programs with great success!

Stage D: End Stage. These are the patients I also see often. If the patient has HFrEF (reduced Ejection Fraction) we are talking about VADs and transplants or continuous milrinone infusion. If they have HFpEF (preserved Ejection Fraction), we have to increase the treatment of all the things that cause heart failure like A-Fib, obesity, diabetes, and hypertension. Even still, exercise can make a huge impact here.

When it comes to End Stage, I tend to see a fair share of VAD patients. Ventricular Assist Devices are mechanical motors installed in the heart (either in the left or right ventricle, or both if you have my patients) to circulate blood. These can be used as a bridge to transplant or as a terminal device and are typically used for patients with a poor ejection fraction (EF). As you could imagine, people with VADs don’t have pulses or blood pressures because they don’t have a pulse… I had the rare opportunity to treat a patient in the home long term who had a Left VAD (EF 21%). It took two years of regular exercise but, you guys, his heart began to recover. The VAD offloaded him enough that his heart began to heal and remodel. By the end of my time with him, I was actually able to take a manual blood pressure and auscultate Korotkoff sounds over the sound of the motor. This is the magic of exercise prescription at work! But I digress…

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Overall, general heart failure management is simple:

The Rule of 2
2 Grams of Sodium
2 Liters of Fluid
2 Pounds of Weight Gain

I’ll break that down:

  • Your patient may only have 2000mg of sodium per day in their diet. This is tough for many patients with HF because much of the food they regularly eat (which is part of what lead them to having HF) comes from a box or a deli counter and is, therefore, HIGH in sodium as a preservative. It’s the American way.
  • Your patient may only have 2000mL of fluid intake in a day. This sounds simple, but I promise you that it is not. Four of those single serving water bottles are equal to 2000mL (they are each 500mL). But patients drink more than water. They drink coffee, soup, juice, and tea. They eat ice chips (really, I promise). So, this does actually become tough to measure.
  • They cannot gain more than 2 pounds in a day (or five pounds in a week). This means that they have to weigh themselves at the same time every day and record this weight for further reflection. This is the practical method of watching for the beginnings of fluid overload. This can be treated if it is caught early and we can avoid an exacerbation and hospitalization.

First step: Refer to a dietician! Let’s be real, we aren’t experts at this stuff. And heart failure comes with its own diet plan! So why not get them directly to the person with that info! The dietician will help them with the sodium part particularly.
Second step: Figure out a method of measuring fluid intake that works for the patient. My favorite is to have a 2 liter bottle on the kitchen counter next to the sink. Every time they want a drink, they fill their cup with that amount of water from the sink, dump it into the 2 liter bottle, and then fill their cup with that same amount of whatever they are drinking. That way, they can watch the bottle fill up over the course of the day and know exactly how much they have to go.
Third Step: Safely getting up on to and down from the scale for daily weights. It always amazes me that no one ever thinks to use their walker. Walk the walker right over the scale and step up on it, let go for a second to measure weight, then grab the walker and keep walking right back down off the scale. Done. Keep the weight log right next to the scale with a pen so they always remember to write it down.

Ongoing Step: Monitor symptoms (lower extremity swelling, shortness of breath, crackles with lung auscultation which could lead to oxygen desaturation with activity, abdominal distention) and check vitals. This we should really be doing anyway! You can use this super handy Red/Yellow/Green light handout for your patient (and yourself) so that everyone knows whats the plan is and what to watch out for! I love that the language is super patient friendly.

Source: Heart Failure Zones from the American Association of Heart Failure Nurses

It’s also important to remember that these guidelines are general. A patient may have more specific restrictions like only being allowed 1.5 liters of fluid intake per day or only 1500mg of sodium per day. Those orders come from the physician so if you don’t see it stated, be sure to check. There is also a caveat to the weight gain/loss rule. If you are exercising your patient to a sufficient intensity, you may see weight gain over time due to gain of muscle mass. You may also see significant weight gain if a patient is recovering from a severe exacerbation that left them unable to eat for a time. Still notify the doctor, that’s their call.

And for the final and most important step in the process….. EXERCISE! You can view the BRAND SPANKING NEW Clinical Practice Guidelines for Physical Therapists in the Treatment of Heart Failure for all the information you’ll need on that! You can read about more specifics HERE.

What is your method of teaching patients how to monitor their fluid intake? Tell me about it in the comments!

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Cleveland Clinic. (2020). Heart Failure: Understanding Heart Failure: Management and Treatment. Retrieved from

Shoemaker, M. J., Dias, K. J., Lefebvre, K. M., Heick, J. D., & Collins, S. M. (2020). Physical Therapist Clinical Practice Guideline for the Management of Individuals With Heart Failure. Physical therapy100(1), 14–43.

American Association of Heart Failure Nurses. (2017). Zone Tool for Heart Failure. Retrieved from

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Chronic Disease Part 1: Heart Failure

Ya’ll know how much I love freeing the yoke! Chronic disease is a huge burden to the general population. This post is the first in a series of posts addressing some of the major chronic diseases placing a yoke around the necks of our patients. We will discuss what these diseases are, what causes them, and what we can do about it! I’ll help you with what you need to know before you go. Let’s talk about one of the major culprits: Heart Failure.

In 2012-2013, new terminology was adopted for the description of heart failure types. Even though it is not widely used, the new language has increased awareness of and research on diastolic dysfunction and opened our eyes to the two major types of heart failure. We used to just think “left” or “right” or “both”, and that wasn’t exactly wrong, but heart failure is more complicated than that, so the terminology needed to be a better descriptor of what was actually going on.

Heart Failure reduced Ejection Fraction (HFrEF)

Also classically known as systolic heart failure, Heart Failure with Reduced Ejection Fraction indicated that the patient has an Ejection Fraction of <40%. In patients with this diagnosis, EKG abnormalities are more common, indicating that heart rhythm issues are present. HFrEF is clearly associated with coronary heart disease (CHD). HFrEF is typically caused by:

  • Myocardial Infarction
  • Viral myocarditis
  • Physical damage to the heart tissue

Damage to the actual cardiac muscle, electrical, valvular, or vascular tissue is what reduces the ejection fraction in these patients. Either the pump can’t pump as hard (left ventricle), the electrical function is interrupted which results in incoordination and decreased strength of contraction (left ventricle), the valve can’t close and open properly so blood slips out when it isn’t supposed to, or the coronary vasculature can’t supply the oxygen and nutrients to the musculature that it requires. In some of the more long-term causes, blood pools up in the left ventricle, stretching the muscle beyond it’s optimal length and reduces the strength of contraction.

This heart failure is typically more of sudden onset which can result in patients having increased difficulty coping and managing the symptoms. Thankfully, because it typically has a sudden onset, the heart musculature doesn’t have enough time to atrophy before rehab professionals are able to intervene. So, although the patients with this type of heart failure may struggle emotionally or mentally with their new diagnosis, their physical function is less limited after initial diagnosis. This is, of course, dependent on the degree of infarction or physical damage.

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There are some in the category who do have significant physical damage or require longer term treatment, such as with viral infections. They may be significantly debilitated due to PICS. Sometimes, this condition is caused by long term disease which results in a larger level of damage, especially if the diseases are left uncontrolled for a longer period of time. Causes of this kind of damage can include:

  • Hypertension
  • Coronary Artery Disease (CAD)
  • Mitral Regurgitation
  • Aortic Stenosis

This is a great population for us to jump in with. These are the folks that are still feeling pretty ok. They know they are going to be facing difficulties, but they typically are ready to go on the rehab to prevent HFrEF from affecting them for as long as possible. They can also undergo procedures to correct for some of these issues (like TAVR procedures for valve repairs). But for hypertension and CAD, prevention is key. One of my patients with HFrEF diagnosis had to be discharged early from home care services because he had reached his only self-selected goal which was to go kayaking with his grandsons. All the warm and fuzzies. We still transitioned him to outpatient cardiac rehab for long term management, though.

Heart Failure preserved Ejection Fraction (HFpEF)

In Heart Failure with preserved Ejection Fraction, the left ventricle of the heart cannot properly fill with blood. Overall, less blood than “normal” still leaves the heart, but 55% or more of the blood in the left ventricle still leaves the chamber. Therefore, the ejection fraction is maintained, but the cardiac output is still less. The ventricle can still pump well but the ventricle walls may be very stiff, so cannot relax enough to fill properly during diastole. This can also happen is the heart wall muscle becomes too thick and the chamber no longer holds as much blood. HFpEF can be diagnosed if the ejection fraction is anything greater than 40%. HFpEF is more likely in females and renal failure a more common comorbidity. Causes include:

  • Long term hypertension
  • Complication of uncontrolled diabetes or long term diabetes (severely stiffened arteries systemically including coronary arteries)
  • Failure/Sarcopenia due to debility and/or obesity
  • Hypertrophic Cardiomyopathy
  • Aortic Stenosis
  • Pericardial Disease (abnormalities of the sac surrounding the heart)

As you can see, many of the causes are the same as HFrEF. That is because the development of these conditions depends on the systemic condition of the person, comorbidities, overall physical level, and many other factors. However, the difference here is that HFpEF is typically caused by long term chronic diseases, which means that I’ve seen a lot of these patients.

The difficulty with treating HFpEF is that these patients ride the long slow train down the very slight decline. There can definitely be a triggering event that starts the train ride, but it is all down hill. The burden of chronic disease takes its toll on their body and the recovery process involves riding that long slow train back up the hill. This takes a lot of time and a lot of effort on the part of the patient and the therapist. The other hard piece to the puzzle is that we don’t usually get to intervene here until much later in the disease process which means there has been systemic muscle atrophy, multiple system failure, and ongoing difficulty with chronic disease management. These patients require a good deal of monitoring at all times when participating in activity because they tend to have a very low overall tolerance.

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The medication burden to the patient with HFpEF is also much higher and more difficult to sustain. They are typically treated with mineralocorticoid receptor antagonists (spironolactone or eplerenone) which cause hyperkalemia, as well as other medications that elevate potassium, so potassium level and intake must be monitored regularly. Have you ever heard of Milrinone? Nasty business… And then add in that they may also require hemodialysis three days per week due to the associated renal failure, and the physical, mental, and emotional toll of that… I have tons of research on that but we will address ESRD in another post.

This all means that, as the physical therapist, exercise may not be the best or only intervention you are providing. This also means that you have some serious considerations for whole-patient management that go far beyond your assessments and interventions. Let’s talk about some of those things…

The treatment is still exercise!

Regardless of the type of heart failure, the treatment is the same: MOVE! Where you start is definitely going to differ based on acuity and type. More acute HFrEF may need phase 1 cardiac rehab interventions, but may progress to stage 3 quickly and be on their merry way. However, patient with HFpEF will be in phase 2 for a very long time and may meander across stages and settings of care. They typically endure a relapsing/remitting disease course that places a large burden on themselves and their caregivers. Baseline functional assessments and outcome measures are critical for patients with HFpEF because progress is long and labored so maintaining skilled care can be more difficult.

Straight from the Clinical Practice Guideline, here is the exercise prescription patients with heart failure need. Please observe those RPE levels… that’s right… 90-95% peak workload is your target.

Physical therapists must prescribe aerobic exercise training for patients with stable, NYHA Class II-III HFrEF using the following parameters: Time: 20–60 min; Intensity: 50%–90% of peak VO2 or peak work; Frequency: 3–5/wk; Duration: at least 8–12 wks; Mode: treadmill or cycle ergometer or dancing (Evidence Quality I; Recommendation Strength: A—Strong) 
Physical therapists should prescribe high-intensity interval exercise training in selected patients for patients with stable, NYHA Class II-III HFrEF using the following parameters: Time: >35 min; Intensity: >90%–95% of peak VO2 or peak work; Frequency: 2–3/wk; Duration: at least 8–12 wks; Mode: treadmill or cycle ergometer. HIIT total weekly exercise doses should be at least 460 kcal, 114 mins, or 5.4 MET-hrs. (Evidence Quality I; Recommendation Strength: A—Strong) 
Shoemaker, M. J., et al. (2020)

There is also plenty of information on the strengthening of the muscles of respiration using IMT training and proper prescription of resistance training. Dr. Shoemaker and his crew even provide the guidance for combining all the different types of training so you can get it all in. We will get in to more details of High-Intensity Interval Training in another post. I’m super excited about that!

Other than exercise…

Keep in mind all the things we talked about in the post about the Rule of 2s! All of these things still come in to play for every one of these patients. Many patients with HFrEF don’t receive the education on how to manage their heart failure using the Rule of 2 because they tend to go quickly in and out of treatment, but that doesn’t mean they don’t need it! If they want to get back to their normal life and live it the best they can for as long as possible, they need to manage themselves properly to prevent decompensation and be healthy enough to participate in exercise or activity-based interventions.

Yes, that means you need to take your patient’s weight. You need to check their weight log. You need to listen to their lungs at every visit and know what you are listening for. You need to check their heart rate (manually, because they have rhythm issues, remember?), blood pressure, and pulse oximetry before, during, and after activity. And if you are in the outpatient setting, you definitely need to do this. Just because someone walked in to your clinic today doesn’t mean they are healthy. That 72-year-old man here for a basic knee evaluation may have knee pain from joint effusion resulting from lower extremity edema secondary to fluid overload. I’ve seen it. This is chronic disease management. Within our scope, within our ability = our responsibility.

For more specifics on treating patients with heart failure, please take a read on the BRAND SPANKING NEW Clinical Practice Guideline for Physical Therapists Managing Heart Failure!

What baseline functional outcome measure is your “go-to” for patients with heart failure? Tell me in the comments!


Black, H. R. & Pitt, B. (2015). HFpEF: The ‘New’ Heart Failure. Commentary for MedScape. Retrieved from /838790#vp_3

Ho, J. E., Gona, P., Pencina, M. J., Tu, J. V., Austin, P. C., Vasan, R. S., Kannel, W. B., D’Agostino, R. B., Lee, D. S., Levy, D. (2012). Discriminating clinical features of heart failure with preserved vs. reduced ejection fraction in the community. European Heart Journal. 33(14):1734–1741.

Oktay, A. A., Rich, J. D., & Shah, S. J. (2013). The emerging epidemic of heart failure with preserved ejection fraction. Current heart failure reports10(4), 401–410.

Pai, R. K., Thompson, E. G., Gabica, M. J., Husney, A. (2019). Heart Failure With Reduced Ejection Fraction (Systolic Heart Failure). HealthWise. Retrieved from,less%20than%20the%20body%20needs.

Pai, R. K., Thompson, E. G., Gabica, M. J., Husney, A. (2019). Heart Failure With Reduced Ejection Fraction (Systolic Heart Failure). HealthWise. Retrieved from

Shoemaker, M. J., Dias, K. J., Lefebvre, K. M., Heick, J. D., & Collins, S. M. (2020). Physical Therapist Clinical Practice Guideline for the Management of Individuals With Heart Failure. Physical therapy100(1), 14–43.

Follow @DoctorBthePT on Twitter for regular updates!

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