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…

Postural Drainage

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

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

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

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

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


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

Isn’t COVID-19 just a respiratory disease? If only that was true. We are good at treating respiratory infections. We have lots of drugs for viral, bacterial, parasitic, and fungal infections of the lungs. Most of them work really well! We also have several back-up treatments, inhaled medications, and adjuvant therapies (like rehab!) that make primary treatments even more effective. We are pretty darn good at treating respiratory infections. So, if COVID-19 was a respiratory disease only, we would have been all over that. We’ve been battling influenza in varying forms for over a century. We’ve stopped pneumonia in its tracks in even the most fragile patients. So, why haven’t we been able to put a cork in COVID-19? The answer is NO, it isn’t just a respiratory disease.

Yes, influenza can give you muscle aches. Yes, pneumonia, if left untreated, can lead to sepsis. But, COVID-19 causes severe physical damage to multiple organs and systems in your body. Particularly susceptible are the kidneys, heart, and brain. It is thought that their susceptibility is due to their expression of ACE-2 receptors, something this coronavirus is eager to find. Even the blood-brain barrier can’t keep it out, because this coronavirus destroys the barrier. The pancreas, skin, and blood vessels are also at particular risk.

We’ve talked about these topics quite a bit in the several previous posts. What do I have to offer that is new? I’m going to start treating COVID-19 like a multi-system disease. Just like we treat diabetes, just like we treat heart failure, just like we treat most other chronic diseases. Notice how I mention “chronic” disease? That’s intentional. That’s because we really don’t know what the long term effects of COVID-19 are going to be. Many people who didn’t require any medical intervention are several months out now on their infections and are still experiencing symptoms such as shortness of breath with little to no activity, and other symptoms that just keep lingering. Many experts feel that the damage this coronavirus causes to the endothelium (the lining of the vessels) will cause a long term increased risk for blood clots and strokes. As rehab providers, we need to know if someone has had COVID-19 because we will want to keep this in the back of our minds when performing our differential diagnosis.

Researchers are finding elevated inflammatory markers in people who have had COVID-19 including C-reative protein and interleukin-6. These are the same inflammatory markers we blame for so many long term inflammatory conditions in people who have end-stage renal disease (ESRD). Down to the cellular level, this disease changes our physiological function, interfering with the renin-angiotensin-aldosterone system (RAAS). This hormone based system also helps regulate inflammation, fluid levels, and blood pressures. People who have heart failure depend on regulated fluid levels in their body, so upsetting this already debilitated system would cause them serious harm.

Photo by Anna Shvets on

Sure, we can treat the inflammation with dexamethosone. We can pump you full of antibiotics to prevent opportunistic infections. We can give you antivirals to slow the damage. We can thin your blood down to water and hope it still carries oxygen. We can treat the breathing problems with budesonide. Heck, we just can breathe for you. We can put you out so you don’t feel a thing. We can filter your blood for you. We can circulate your blood for you. We can flip you over so you breathe better. We can even wake you up just a little bit and walk you around the room attached to 30 different machines with a team of 8 or more highly skilled medical providers… But my goodness, we’ve never really had to do all of that at one time for one single person… And now we are doing it for thousands of people at hundreds of facilities all over the world.

Not a single one of those treatments is the answer. Every treatment that is hailed as the next “magic” answer to COVID-19 doesn’t address the whole disease. It may address part of it, like the early phase with minimal symptoms, or the asymptomatic phase, or the late acute phase, but nothing addresses all of it. We can definitely cut the mortality rate, which is a huge step, but no single treatment has been enough to prevent it all together. People who otherwise take these “hailed” medications for pre-existing medical conditions still contract COVID-19. The burden of this disease is huge and we have only seen a few months worth of damage.

Don’t get me wrong. I WANT there to be a cure or treatment or something that is effective at just wiping this thing out. We’ve done it with other viruses and bacteria through vaccines (like with Polio and Pertussis) or engineering controls like water sanitization (for Cholera). I’m also not saying a vaccine is the answer. What I’m saying is, I’m not ready to jump to conclusions about a single drug or treatment. Evidence, research, and time are important. We could find the greatest thing ever that treats everything perfectly, but then down the road we find it has side effects even worse than what we otherwise would have experienced. This has happened before (remember thalidomide?), and I don’t want it to happen again. Even if we come up with the perfect treatment or preventative tomorrow (fingers crossed!) we still have the people currently experiencing COVID-19 and its sequelae that need quality treatment.

All of this doesn’t mean we know nothing. Quite the opposite! We can actually predict with greater than 90% accuracy what someone’s clinical disease course will be, what levels of care they will need, and what treatments will be the best for them at each phase. We know that COVID-19 isn’t overall that deadly, but we do know that it is very damaging, and either one isn’t good. Polio was pretty damaging, too. We have three new studies confirming airborne transmission is possible and likely, especially in close confines and indoor environments. This research is what informs re-openings, mask wear, and other protective measures. I’d say we actually know quite a bit which is why we now know that this is a multi-system disease that needs to be treated like one.

Treating a Multi-System Disease

If we have a patient with diabetes, we don’t just treat their blood sugar. Even as rehab providers, we look at their circulation, their peripheral sensation, their central and peripheral balance, their cardiac function, their vision, and so many other aspects because we know that diabetes causes impairments in all of these domains. If we have a patient with heart failure, we never just look at their heart, do we? We know they have changes in their kidneys, their lungs, their vasculature, and their muscles… So we use test and measures to address all of these components. This is exactly How we need to be looking at survivors of COVID-19.

In the rehab world, what can we do to address COVID-19 as a multi-system disease? How does this change the way we screen, evaluate, and treat? You will need to look at the whole patient. Even in the outpatient setting, they are not just knee pain who had COVID-19 two months ago. If you are seeing patients in any setting who have had COVID-19, even tested positive but remained asymptomatic, you need to be looking at a number of things and the APTA has summed it up in 5 easy measures:

  1. Physical Function. Can we start out with, “Duh?”. The best way to do that is to use the Short Physical Performance Battery (otherwise known as the SPPB). This is a combination of three already standardized tests (timed chair rise, gait speed, and static balance) that give you raw scores and a sum score that is highly predictive of function. This is a great tool across functional levels and gives you a good amount of functional information to inform and direct your treatments. You can get all the deets here:

2. Strength. COVID-19 is known for causing weakness in the small muscle groups and the core. You may have a patient who can stand, but they can’t write their name. They may do a squat, but can’t walk 10 feet. Anyone who you meet that has had an ICU stay for COVID-19 is at risk for ICU acquired weakness (ICUAW). In that case, the Medical Research Council Sum Score (MRC-SS) is recommend for assessing strength. There are several articles listen in the references for the MRC-SS, but generally it is a combination of manual muscle tests of certain muscle groups.
Here is the source for this file: ResearchGate.

You can also learn more about scoring this was from this video:

3. Endurance. You’ve probably heard by now of someone who had COVID-19 and needed months of rehab. Or who didn’t go to the hospital but still gets short of breath walking short distances. Whether it’s due to long term immobility in the hospital or actual parenchymal damage to the lung tissue (or other body systems), endurance becomes significantly affected. The recommended test for endurance in people who have had COVID-19 is the 2 minute step test. This is a favorite of mine for people of all ages! I’ve used this for my ESRD patients, VAD patients, young athletes, and middle-aged adults. You can download the one-page here:

4. Cognition. We have talked several times about the effects COVID-19 can have on the brain. In this case, you should probably have a tool in your pocket to assess cognition. There are some specific cases of COVID-19 that are associated with delirium lasting longer than 72 hours. In the absence of other serious symptoms, you may find this patient in your clinic for any number of reasons or you may find that one of your current patients starts to develop some strange symptoms. The SLUMs (the Saint Louis University Mental Status Exam) is the recommended assessment to use in this case. You can access it for free here:

5. Quality of Life. Isn’t this what we should always be focused on? What can we do as rehab providers to improve someone’s quality of life? Unfortunately, we so often do not assess or quantify it, so it can be difficult to demonstrate improvement other than subjective report. The ED-5Q-5L is a simple questionnaire that can reliably quantify the quality of life for patients who have had COVID-19. Unfortunately, I can’t give you this one. However, you may be able to get it for free when you register with the company who created it. You can do that here: You can also view a sample of the document in English.

There is your tool box! You’ve got something for every major system. Obviously you can insert other objective measures you may need specific to your patient. For the time being, this is what we’ve got, and I think it’s a pretty strong set of tools. Hopefully, soon, we won’t need to worry so much about all of this, but until that day comes, we will continue to be the frontline against community spread, and the treatment for those with longterm medical complications regardless of their setting.

Have you used any of these tools for assessing patients after a run with COVID-19? Did you run in to any ceiling effects? Tell me about how they did and how they progressed in the comments!

More Reads…

It’s Getting Hot in Here: Body Temperature

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


American Physical Therapy Association. (2020). APTA Academies and Sections Consensus Statement: COVID-19 Core Outcome Measures. Retrieved from

Arshad, S., Kilgore, P., Chaudhry, Z. S., Jacobsen, G., Wang, D. D., Huitsing, K., Brar, I., Alangaden, G. J., Ramesh, M. S., McKinnon, J. E., O’Neill, W., Zervos, M., & Henry Ford COVID-19 Task Force (2020). Treatment with hydroxychloroquine, azithromycin, and combination in patients hospitalized with COVID-19. International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases97, 396–403.

Azimi, P., Keshavarz, Z., Laurent, J. G. C., Stephens, B. R., Allen, J. G. (2020). Mechanistic Transmission Modeling of COVID-19 on the Diamond Princess Cruise Ship Demonstrates the Importance of Aerosol Transmission. medRxiv 2020.07.13.20153049. Retrieved from doi:

Bonn, D., Smith, S. H., Somsen, A., van Rijn, C., Kooij, S., van der Hoek, L., Bem, R A. (2020). Probability of aerosol transmission of SARS-CoV-2. medRxiv 2020.07.16.20155572. Retrieved from doi:

Connolly, B., Thompson, A., Moxham, J., Hart, N. (2020). Relationship Of Medical Research Council Sum-Score With Physical Function In Patients Post Critical Illness. American Journal of Respiratory and Critical Care Medicine. 201:A3075. Retrieved from

Connolly, B. A., Jones, G. D., Curtis, A. A., Murphy, P. B., Douiri, A., Hopkinson, N. S., Polkey, M. I., Moxham, J., & Hart, N. (2013). Clinical predictive value of manual muscle strength testing during critical illness: an observational cohort study. Critical care (London, England)17(5), R229.

Kingsland, J. & Sanfins, A. (2020). COVID-19: Doctors round up evidence of damage outside the lungs. Medical News Today. Retrieved from

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Santarpia, J. L., Herrera, V. L., Rivera, D. N., Ratnesar-Shumate, S., Reid, S., Denton, P. W., Martens, J. W. S., Fang, Y., Conoan, N., Callahan, M. V., Lawler, J. V., Brett-Major, D M., Lowe, J. J. (2020). The Infectious Nature of Patient-Generated SARS-CoV-2 Aerosol. medRxiv 2020.07.13.20041632. Retrieved from doi:

Tsui, E. L. H., Lui, C., Woo, P. P. S., Cheung, A. T. L., Lam, K. W., Tang, T. W. , Yiu, C. F., Wan. C. H., Lee, L. H. Y. (2020). Development of a data-driven COVID-19 prognostication tool to inform triage and step-down care for hospitalised patients in Hong Kong: A population based cohort study. medRxiv. 2020.07.13.20152348 Retrieved from doi:

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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.

Photo by Karolina Grabowska on

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 and the toll that takes on a person physically, mentally, and emotionally… 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 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 for 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 be 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 to 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!

Sternal Precautions

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


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

Diaphragmatic Breathing

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


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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.

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Exercise-Induced Hypertension

Have you ever had patient exercising during your treatment session and taken their blood pressure only to find that is has shot up pretty high? They didn’t have symptoms of high blood pressure so you rested them and it came right back down. But, then you find that it keeps happening… What does this mean? Are they just intolerant to exercise due to deconditioning? Not necessarily. Exercise-induced hypertension can happen even in healthy individuals. There have been questions for several years about what exercise-induced hypertension means, and the answers are becoming clear.

So what is a normal blood pressure response to exercise?

We expect systolic blood pressure to rise about 20-60 mmHg during exercise, but this varies from patient to patient and is based on symptomology. It is fairly standard to see a rise of 8-10mmHg per MET of exercise, which eventually plateaus at peak activity level. A better cut off number is 180mmHg. Diastolic blood pressure, however, we need to keep an eye on. We do not want diastolic blood pressure to rise greater than 10 mmHg with activity.

Blood pressure can also drop with exercise, which is actually the long term goal of using exercise to manage hypertension. However, too much of a drop and this does indicate activity intolerance, especially when it drops in conjunction with a drop in heart rate. When blood pressure significantly drops in response to exercise, it can also be an indicator of future cardiovascular events. If systolic blood pressure drops are 10mmHg or more, it is an absolute red flag and any exercise or activity must stop. More of a drop than that can indicate severe active pathology like an active infarction or significant reduction in cardiac output. However, dehydration must also be considered, especially when the patient has diuretic medications on board. We talk about this more in this post.

What is Exercise-Induced Hypertension?

Also known as Exercise HTN, Exaggerated Blood Pressure Response to Exercise (EBPRE), or Hypertensive Response to Exercise (HRE). Exercise-Induced hypertension is an apparently ‘normal’ resting BP (<140/90 mm Hg) but excessively high exercise BP. Specifically, a systolic BP of ≥210 mm Hg for males and ≥190 mm Hg for females and, although less common, a diastolic BP ≥110 mm Hg for both males and females at any exercise workload. It is found in 18% of normotensive people, as much as 40% of hypertensive people, and in more than 50% of people with Type 2 Diabetes Mellitus.

Exercise-induced hypertension can also be defined as a blood pressure greater than the 90th percentile or normal during moderate intensity workload. You can view a table of what is considered 90th percentile of normal blood pressure during exercise here:

Exercise-induced hypertension may be indicative of an early phase of essential hypertension or pre-hypertension, indicates poor left ventricular adaptations and function, and may also be an indicator of poor hypertension control. Exercise-induced hypertension is associated with a significantly higher risk of cardiovascular events and mortality due to these events, even when present in otherwise healthy people without other risk factors.

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What causes exercise-induced hypertension?

So many things…

  1. Metabolic conditions such as diabetes, metabolic syndrome, or high cholesterol, and any other conditions that lead to insulin resistance, vascular stiffness, or atherosclerosis.
  2. Conditions that impair systemic vasculature such as systemic inflammation. Several lab values have been associated with abnormal blood pressure responses to exercise, most of which are markers for inflammation:
    1. C-reactive protein
    2. Albumin-creatinine ratio (kidney function marker)
    3. Interleukin-6
  3. Large artery wall stiffness, such as in the aorta, femoral, or brachial arteries. Stiffness in the large arteries does not allow for proper compliance adjustments when volumes of cardiac output increase to accommodate exercise.
  4. Neurohormonal Vascular Control impairments, such as with traumatic brain injuries or neurodegenerative processes (even just aging). The neurovascular dynamics in response to exercise come primarily from a memory mechanism, not from peripheral changes due to exercise. This is because exercise is an active choice. Peripheral changes due to exercise (from chemoreceptors and mechanoreceptors) will inform these memory responses and further adjust the vasculature as needed. But the initial response is central. If those parts of the brain that hold these memories for how to respond to an increase in activity are damaged, blood pressure could rise unchecked until peripheral responses can catch up. (My inner nerd really came out in this one… I was completely entranced in learning about this!)
  5. Impaired hemodynamics. We will elaborate a little more on this later in the post but, generally, if your are not hemodynamically stable, your blood pressure response to anything is going to abnormal.

What else does the research say?

Although the risk for Exercise-Induced Hypertension is greater in males, it seems to indicate a higher risk of future medical problems for women. An article written in 1985 regarding hypertensive response to exercise in women was recently updated with new information regarding the effects of this phenomenon on women. The authors found that women are at increased risk for heart failure with preserved ejection fraction (HFpEF) largely due to higher prevalence of arterial and cardiac stiffening. The authors also found several pre-clinical indicators of pathology based solely on the exercise blood pressure response.

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In a large longitudinal study, a 36% increase was found in the rate of cardiovascular events and mortality in individuals with an HRE at moderate exercise intensity. In addition, for every 10mmHg rise in systolic blood pressure with moderate intensity exercise, a 4% increase in the risk for cardiovascular events was present. Moderate intensity exercise was defined as stage 1 or stage 2 of an exercise test, OR the intensity of normal daily activities. So, these authors found that just the activity of a normal day was enough to illicit hypertensive responses in healthy people who experienced exercise-induced hypertension.

And here is where things REALLY get weird…

If you are working with patients who have known underlying cardiovascular pathology (NOT hypertension), it is actually PROTECTIVE for them to have an exaggerated blood pressure response to activity! Studies have shown that this is actually an adaptive response of the cardiovascular system to maintain myocardial function (Remember that Frank-Starling Principle we talked about?). When I was researching all of this I kept thinking, “what is this magic?” But as I thought about it, it makes sense because higher pressure helps maintain patency of the coronary arteries to promote improved perfusion for increased workload.

As Physical Therapists, we are the frontline.

The first step? Screening. Dr. Severin and his crew stated, “It is our ethical duty to screen.” We have the tools and the knowledge to screen people for hypertension and should do so every chance we get. To be honest, we typically can tell who is at really high risk for hypertension with a glance at their chart, and we can typically tell who really isn’t at risk for hypertension in the same way. But, what about all those people in between? And what about those completely healthy people who demonstrate exercise-induced hypertension? We have to screen.

“Exercise BP response may be an inexpensive screening tool to identify women at highest risk for developing future HFpEF.”

Sarma, et al. (2020)

Another study found that, in people at risk for hypertension who had normal resting blood pressures and no exercise-induced hypertension, lifestyle modification was enough to significantly reduce the development of hypertension at 1 year post-intervention. However, if exercise-induced hypertension was already present, lifestyle modifications were not enough, and long term exercise had to be part of the intervention to reduce the risk.

“it seems mandatory to mutually promote early diagnosis/treatment of exaggerated blood pressure response to exercise in healthy subjects without hypertension and encourage physical activity in prevention, treatment, and control of all stages of hypertension.”

Calderone, et al. (2017)

A randomized controlled trial showed that 12 weeks of treadmill-based exercise training could improve both ambulatory and exercise BP measures in individuals with resistant hypertension (defined as uncontrolled BP despite the use of ≥3 antihypertensive medications, including a diuretic). Can you imagine? Being on 3 or more blood pressure medications at the same time and STILL having hypertension? I can see the orthostasis from here! I’ve actually had several patients in exactly this situation. Hopefully, people are able to attempt treatment of their hypertension with exercise and/or lifestyle modifications first, but let’s be honest, this rarely happens. Patients are almost immediately placed on ACE inhibitors and then eventually beta-blockers when they have hypertension in isolation. But, when the pharmaceutical route fails, it’s up to us.

“In fact, there is an the ample evidence in the literature that physical activity could positively affect endothelial function, arterial stiffness, neurohormonal response and finally blood pressure levels both in healthy men and in hypertensive patients and so should be considered a very important element in the prevention and management of cardiovascular disease.”

Calderone, et al. (2017)

Prescribing the appropriate intensity and time of exercise to be therapeutic for managing hypertension is essential. According to ACSM, people with hypertension should exercise at a moderate intensity (3-5/10 or 12-14/20 on the Borg Scales or 3-6 METs) aerobic exercise 5-7 days per week. In addition, they should also perform dynamic resistance exercise 2-3 days per week and flexibility exercise 2-3 days per week. A minimum of 30 minutes and maximum of 60 minutes per bout is sufficient, OR, if utilizing HIIT exercise, 10 minutes bouts. This is because regular aerobic exercise results in reductions in blood pressure of 5-7 mmHg among individuals with hypertension and these reductions translate to a reduced risk of CVD of 20-30%. You may need to start small and progress gradually to achieve this with your patients if they are more debilitated OR at a higher risk of cardiovascular event. BUT, the effects are dose-dependent, so if you don’t reach the therapeutic threshold, you won’t see results.

Exercise blood pressure should be measured at every patient treatment. The reality is, you are going to be the only person who even has the opportunity to measure someone’s blood pressure during exercise BEFORE they experience a cardiovascular event. You will be the only one who had the opportunity to detect exercise-induced hypertension before it manifests as something more treacherous. Take the opportunity because it could very literally save the life of the person in front of you.

How many people have you encountered that have exercise-induced hypertension? What were their clinical characteristics? Tell me in the comments!

More Reads…

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

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

Vibration & Percussion

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

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

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


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Caldarone, E., Severi, P., Lombardi, M., D’Emidio, S., Mazza, A., Bendini, M. G., & Leggio, M. (2017). Hypertensive response to exercise and exercise training in hypertension: odd couple no more. Clinical hypertension23, 11.

Dimeo F, Pagonas N, Seibert F, Arndt R, Zidek W, Westhoff TH. Aerobic exercise reduces blood pressure in resistant hypertension. Hypertension. 2012;60:653–658. Retrieved from

Kim, D., & Ha, J. W. (2016). Hypertensive response to exercise: mechanisms and clinical implication. Clinical hypertension22, 17.

Le, V., Mikitu, T., Sungar, G., Myers, J., Froelicher, V. (2008). The Blood Pressure Response to Dynamic Exercise Testing: A Systematic Review. Progress in Cardiovascular Diseases. 51(2):135-160.

Mayo Clinic. (2019). Exercise: A drug-free approach to lowering high blood pressure. Retrieved from

Sabbahi, A., Arena, R., Kaminsky, L. A., Myers, J., & Phillips, S. A. (2018). Peak Blood Pressure Responses During Maximum Cardiopulmonary Exercise Testing: Reference Standards From FRIEND (Fitness Registry and the Importance of Exercise: A National Database). Hypertension (Dallas, Tex. : 1979)71(2), 229–236.

Sarma, S., Howden, E., Carrick-Ranson, G., Lawley, J., Hearon, C., Samels, M., Everding, B., Livingston, S., Adams-Huet, B., Palmer, M. D., & Levine, B. D. (2020). Elevated exercise blood pressure in middle-aged women is associated with altered left ventricular and vascular stiffness. Journal of applied physiology (Bethesda, Md. : 1985)128(5), 1123–1129.

Schultz MG, Hordern MD, Leano R, Coombes JS, Marwick TH, Sharman JE. (2011). Lifestyle change diminishes a hypertensive response to exercise in type 2 diabetes. Med Sci Sports Exerc. 43(5):764-9. Retrieved from

Schultz, M. G., & Sharman, J. E. (2014). Exercise Hypertension. Pulse (Basel, Switzerland)1(3-4), 161–176.

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

Weiss, S. A., Blumenthal, R. S., Sharrett, A. R., Redberg, R. F., & Mora, S. (2010). Exercise blood pressure and future cardiovascular death in asymptomatic individuals. Circulation121(19), 2109–2116.

WHO. (2020). What is Moderate-intensity and Vigorous-intensity Physical Activity?

Zaleski, A. (2019). Exercise for the Prevention and Treatment of Hypertension – Implications and Application. American College of Sports Medicine. Retrieved from

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

This post is written for one and all. If you are not a rehabilitation or medical professional, please read this post. Even if you are, please read this post. I’m going to address some things that need clarification. You can have all the opinions you would like, but there are some things that are just facts. Not opinions, not choices, not beliefs. Facts will continue to exist whether or not you believe in them. Facts can and do change contextually and over time, but not based on someone’s opinion of them. They change in response to a change in evidence, science, and environment.

Today I’m going to provide you with some old evidence and old science. The reason for that is two-fold. First, it’s because masks are OLD! We’ve been using them for a long time. The second is because I didn’t want to use any single bit of research that was influenced by the environment of COVID-19. The world view of science has become terribly distorted in the last year so I’ve only used research from before the time of “alternative facts” and just used facts. Keeping it simple.

The other day, I met a young woman who described herself as, “someone other people don’t like,” because she doesn’t wear a mask. She then said that even when she worked in the hospital, she just “didn’t like” wearing them. She then attempted to get me to agree with her that, “well, you work in healthcare, you know they don’t work. They stop droplets but they don’t stop the virus.” She then told me that 30 of her friends have COVID-19 from a large camping trip and are very sick and that she wouldn’t wish it on anyone.

Let me make this perfectly plain:


  • They work best when used in conjunction with other methods of infection control.
  • Different types of masks work to different levels and nothing is perfect. Not all masks, and not even all surgical masks, are created equally.
  • Masks that are not worn properly work less.

This person I met who “worked in a hospital” is spreading fallacies and doesn’t understanding virology, infection control, or public health concepts. She is also terribly confused based on her story of her friends’ illnesses. I’ve heard so many arguments against masks by people from all walks, medical or not, science or not, government or not. But here are the facts:

How and Why do Masks Work?

To answer that, we have to discuss the Chain of Infection. There are 6 links, which are pictured below. At any point, we as humans can insert ourselves or our interventions in to the chain to reduce or stop the infection risk.

Step 1: You can’t get sick if there isn’t a microbe around to get you sick. This is where engineering controls can really make a difference. Proper ventilation, cleaning, and other engineering controls remove infectious agents and, therefore, remove the risk of infection.

Step 2: You have to have an infectious source. This would be the person who is infected. This person, if they were aware that they were sick or contagious, could stay home and away from others, not sharing what they have and then the infection dies without being passed to another person. Antibiotics, antivirals, antifungals, and antiparasitics can also intervene here. Kill the infectious agent in the host so it can’t spread.

Step 3: The microbe has to exit the person who is sick. Some viruses have very specific ways they can leave the body, such as only through certain bodily fluids. HIV is one of these viruses. Many body fluids do not serve as a means of exit for HIV, only certain ones (blood, etc.). In conditions like tuberculosis, the microbes are spread in the air by the infected person breathing (respiratory droplet nuclei). The infected person would likely have a hard time keeping a respiratory microbe inside their body and they symptoms typically produce coughs or sneezes, so engineering controls can be helpful here again, OR the person can block the exits of their body by using a mask to prevent the spread of microbes to others. Some microbes that don’t require respiratory transmission, like sexually transmitted viruses, are blocked by other barrier devices.

Step 4. The microbe has to have a means of contact to another person. It can’t just be any contact, it has to be the specific type of contact that the microbe requires. The microbes on your hands have to get to your eyes, nose, mouth, or whatever they can infect. If you utilize interventions such as washing your hands, that may never happen. Some microbes linger in the air (like we discussed above with tuberculosis) and have to be breathed in. This is also where barrier devices are useful. You can wear a barrier device to protect yourself.

Step 5. Once the microbe has made contact, it must access the type of tissue in your body it is able to infect. So, just because you became that person in step 4 who had contact with droplets on your hands, doesn’t mean you’ll contract an illness, unless your then put your hands in your mouth or rub your nose. Once this happens, the microbes have entered your body. There are a few things that can prevent this from happening including PPE. Healthcare workers know we are going to make it through step 4 on a daily basis, so we wear gloves, gowns, shields, and other pieces of equipment to ensure that the droplets that do land on us can’t cause infections. We throw all that stuff away so the droplets don’t contact any part of us.

Step 6: Once the microbe has entered the body, the immune system goes to work. But if the immune system isn’t strong enough for any reason, it will become easily overwhelmed. This doesn’t necessarily have to be a weakened immune system, either. Sometimes, microbes are able to overwhelm even healthy immune systems. That’s why even healthy people get sick sometimes. Some microbes are just really good at what they do. People who do have weakened immune systems sometimes take antibiotics every day to help fight off infections that find a way in.

Specific to COVID-19…

In the specific case of COVID-19, the virus can’t magically travel from person to person on its own. As a respiratory pathogen, it has to be carried on droplets or droplet nuclei that are breathed out, coughed out, sneezed out or spit out in one way or another (these are called “aerosol generating procedures“). The spread of both droplets and droplet nuclei are significantly reduced by a mask. Because people may not know they are infected, we automatically skip to step 3 in the chain of infection. Once the virus exits the body of the carrier by one of these methods, it is transmitted to those around them. Masks then reduce the ability of someone else’s droplets to land in your nose or mouth because they are covered. This is why protection is a 2-way Street. If your mouth and nose are uncovered, my droplets have a higher chance of landing in your mouth and nose and your droplets have a higher probability of making it to me. Like I said, nothing is perfect, but the mask helps reduce the risk.

Something I see brought up often is that healthcare providers are wearing masks, but they still get sick. This is where we need to consider is viral load. The more people you come in contact with who have any viral illness, the higher your viral load. And remember, with COVID-19, the majority of people are asymptomatic carriers. But, we also know that with COVID-19, the more exposure to the virus, the more severe the disease presents. Wearing a mask significantly decreases your viral load, allowing your body to fight a smaller amount of virus so can remain healthy. It allows your immune system to do its job without being overwhelmed by the infection. So, yes, medical providers wear masks and still get sick. That is because we take on a much higher viral load, especially in the emergency care and ICU settings, because so many of the people medical providers come in contact with have COVID-19. You are in lesser contact in the community because those people aren’t showing that they are sick. Only patients showing symptoms, who are much more likely to carry disease, seek medical care.

Here is another example:
In the world of wound care, we have patients wash wounds with soap and water, or sometimes specific agents, to reduce the bacterial load on their wounds. If the wound is already infected, washing it reduces the work the body has to do to fight off the infection. In other words, it supports immune function. If the wound isn’t infected yet, reducing the bacterial load helps the wound not get infected because the immune system doesn’t get overwhelmed and can continue to do its job.

For more information about viral load, engineering controls, and different levels of infection control, please check out this post! PPE is the WORST!

But I can’t breathe in a mask!

If you know me, you probably know that I spent years working with people pre- and post-lung transplant who were at the end stage of lung disease. They were literally days away from suffocating to death. After transplant, they were on immunosuppressant drugs for the rest of their lives. All of these people wore masks whenever they went out to protect themselves because one bout pneumonia from someone else’s droplets could kill them. One outing in too much pollen could land them on a ventilator. One day of their neighbor running a wood stove could mean a week in the hospital. I also work with people who have end-stage COPD, heart failure, pulmonary fibrosis, and all other manner of heart and lung diseases. These people are wearing masks every day while in our facilities to protect themselves. My incredibly sick or immunocompromised people can breathe just fine in their masks, even while I make them do therapy.

Schroedinger’s Mask

We need to understand that it is not possible for masks to be so effective at blocking air that people can’t breathe, while simultaneously being completely ineffective at blocking a virus. Like I said, even my very sick patients can still breathe while exercising in their masks! This is because surgical masks filter at about 5 micrometers (the average size of those droplets we talked about). Carbon dioxide (CO2) has a diameter of 116 picometers and Oxygen is 152 picometers so they are breezing through your mask without a problem. Surgical and cloth masks do not seal to your face, and provide ample room for oxygen and carbon dioxide to leave the breathing space. An N95 respirator filters at about 0.3 micrometers, or 300,000 picometers, so CO2 and oxygen flow right through those also. If you have high carbon dioxide content in your blood, you probably have an underlying lung disease (like my patients) and a mask won’t change this. Several physicians have taken their own and others’ arterial blood gases after a full shift of wearing an N95 to find that their PaCO2 (the amount of carbon dioxide in their blood) is completely normal.
For those not familiar with the comparison: 1 nanometer = 1000 picometers. Here is a chart:

SARS-COV-2, the virus that causes COVID-19, has a diameter of 60-140 nanometers. That means that the SARS-CoV-2 virion is exponentially larger than a CO2 molecule, yet still small enough to get through even an N95. That doesn’t mean they can’t be filtered! Like I explained above, the virion can’t just magically move from person to person. It has to be carried on a droplet or droplet nuclei. Droplets are about 5 micrometers on average, which is why surgical masks filter at this rate. N95s filter at 0.3 micrometers because this is the average size of droplet nuclei. Yes, cloth masks are different, but still can block large droplets and significantly reduce all droplet spread so they don’t come in contact with other people (remember the links on the chain!).

For the medical folks…

There was a Cochrane review performed in 2014 regarding the effectiveness of surgical facemasks at preventing infection. This review showed that there was no statistically significant difference in infection rates between the masked and unmasked group in any of the trials when worn during surgical procedures. (WHAAATT?!?!) I know, but this review was discussed at length by several authors and there are some important things to point out, specifically that only 3 studies could even be included because NO ONE WANTS TO BE THAT SURGEON! One of the discussions had this to say:

“when current surgical practice is the culmination of layer upon layer of precautions in the hope of preventing surgical site infection, do we dare to experiment with their omission to see if they have any tangible consequence on morbidity and mortality? “

Da Zhou, et al. (2015)
Well, of course, someone dared…

A few randomized controlled trials attempted to remove any single step in the operative infection control process to terrible detriment of the patients. Many of the studies had to be stopped because so many people were getting sick that the studies could no longer continue. The overall picture is that surgeries are highly infection controlled: from the pre-operative antibiotics to the ventilation systems to the pre-surgical scrub-ins to the sterilization procedures, so what single piece of this process that contributes most to infection prevention is hard to know because they all work together. Just like infection control in the larger population, it requires more than one step.

What I’m trying to say is that you are going to have a very hard time explaining to me why you can’t wear a mask unless you are a child under 2 years old. My colleagues from 24 to 61 years old are running with masks on daily without oxygen desaturation. Medical providers (myself included) are working 8-12 hour shifts with masks on and not desaturating. We are moving and lifting equipment and human beings repeatedly while we wear them. Transplant surgeons wear their masks for 14 hours straight while swapping new lungs in to a human being. Does that mean we aren’t uncomfortable at times? No! Do we like wearing masks? No, absolutely not. But, like I tell everyone else, liking it is NOT a requirement.

“It is important not to construe an absence of evidence for effectiveness with evidence for the absence of effectiveness. While there is a lack of evidence supporting the effectiveness of facemasks, there is similarly a lack of evidence supporting their ineffectiveness.”

Da Zhou, et al. (2015)

To this day I have only heard of a few legitimate medical reasons to not wear a mask: 1. A patient had multiple facial and skull fractures from a car accident that caused extreme pain from the ear loops and an inability to get coverage of the nose and mouth. His Occupational Therapist found something else for him to wear instead.
2. Emotional trauma from abuse or neglect involving covering of the nose/face/mouth resulting in anxiety, panic attacks, or other mental health conditions.

Remember, I have worked with the sickest of the sick and those at the end stage of lung disease. These people have significant physical and mental trauma from being constantly in fear of suffocating to death at any moment. If they can wear a mask for three hours of medical appointments while on 14 liters of oxygen, then most people can wear them for a 15 minute trip to the grocery store. There may be a few other exceptions that I haven’t yet come to know, but for these few that have difficulty (not that they CAN’T wear a mask for a short time, it is just difficult for them), the rest of us have to do our part to break the chain for them by following the rest of the steps. We have to keep each other safe.

UPDATE as of September 1: I have yet to encounter any other examples were a mask would not be possible. Still waiting…

Got some ABGs you want to share? I’m all ears! Throw them in the comments!

More Reads…

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

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


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Chughtai, A. A., Seale, H., MacIntyre, C. R. (2013). Use of cloth masks in the practice of infection control – evidence and policy gaps. International Journal of Infection Control. 3(9):1-2. Retrieved from

Da Zhou, C., Sivathondan, P., & Handa, A. (2015). Unmasking the surgeons: the evidence base behind the use of facemasks in surgery. Journal of the Royal Society of Medicine108(6), 223–228.

Lipp, A. and Edwards, P. (2014). Disposable surgical face masks for preventing surgical wound infection in clean surgery. Cochrane Database Syst Rev. 2: CD002929.

MacIntyre, CR; Chughtai, AA (9 April 2015). “Facemasks for the prevention of infection in healthcare and community settings”. BMJ (Clinical Research Ed.)350: h694. doi:10.1136/bmj.h694PMID 25858901.

Royal College of Nursing. (2016). The Chain of Infection. Retrieved from

Follow @DoctorBthePT on Twitter for regular updates!

Open Heart, Open Mind

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

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

And I said, “Huh?”

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

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

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

What kind of side effects are we talking here?

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

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

What Does this Mean for Us?

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

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

Photo by Anna Shvets on

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

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

Is there anything else I need to know?

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

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

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

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

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

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

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

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

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

More Reads…

Open Heart, Open Mind

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

Blood Pressure Basics

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

ABGs (Part II)

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


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

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

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

Follow @DoctorBthePT on Twitter for regular updates!

Blood Pressure Basics

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

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

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

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

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

Resting Blood Pressure: the basis for all decision making


1. Patient position:

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

2. Cuff size and positioning:

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

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

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

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

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

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

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

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

Performing Repeat Measures and Side-to-Side Comparisons

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

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

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

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

Can’t I Just Use An Electronic Cuff?

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

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

Freeze, et al. (2011)

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

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

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

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

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

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

Severin, et al. (2020).

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

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

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

AHA, 2017

The “What Ifs” of Taking Blood Pressure

What if…

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

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

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

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

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

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

More Reads…


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

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

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

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”


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

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

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

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

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

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

Follow @DoctorBthePT on Twitter for regular updates!

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ABGs (Part II)

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

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

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

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

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

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

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

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

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

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

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

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

Practice 1:

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

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

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

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

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

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

Practice 2:

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

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

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

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

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

Ready for one more?

Practice 3:

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

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

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

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

Characteristics of acid-base disturbances

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

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

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

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

More from the Pulmonary Rehab Toolbox…

ABGs (Part 1)

This is the first post in a two-part series about understanding and interpreting arterial blood gases! If you want the rest of the post, you’ll have to check back next week! I’m getting real science-y again! So, just a heads up: my undergraduate degree was in chemistry. Kind of by accident, I took a lotContinue reading “ABGs (Part 1)”

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

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

Follow @DoctorBthePT on Twitter for regular updates!


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

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

Photo by Gustavo Fring on

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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


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

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

Photo by Renzy Atibagos on

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

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

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

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

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

Be careful out there.

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

More Reads…


Also known as prior level of function in case you aren’t in to abbreviations. How many times have you written that today? This week? This month? How much thought have you given to what PLOF actually looks like for that patient? Isn’t their PLOF why you are seeing them in the first place? Let’s unpackContinue reading “PLOF”


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

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

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

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

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

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

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

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

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

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

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

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

Follow @DoctorBthePT on Twitter for regular updates!

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

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

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

Photo by Anna Shvets on

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

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


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

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

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

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

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

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


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

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

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

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

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

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

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

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

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