The Beta Blockade

Ugh, medications… I know, I know. I will try to make this as painless as possible. This one matters. It REALLY matters. For patients who have COVID-19 and for patients who don’t. Please take a quick read. Let’s start off by asking some questions.

What does a β-blocker do?

  • Blocks norepinephrine and epinephrine from binding to beta receptor sites (β1, β2, and β3 receptor sites), increases parasympathetic responses by blocking sympathetic input
  • Primary uses: Reduce heart rate, reduce blood pressure, vessel dilation, regulation of abnormal heart rhythm, reduce myocardial oxygen demand.
    • Overall decrease in mortality and morbidity.
    • Decrease abnormal ventricular remodeling of cardiac muscle tissue due to disease states.
  • Adverse effects: airway constriction, sudden heart failure, shortness of breath (in asthmatics), masking of low blood glucose symptoms in diabetics
  • SAFETY LIMIT: MediSpan and other medication management tools limit medication that effect blood pressure to four per patient. If this number is exceeded, risk of orthostasis is significant. Beta blockers would be included in this limit.

β-receptors? Can someone remind me what those are for?

Why sure!
β1 receptors on the heart increase heart rate, heart contractility, and cardiac muscle conductivity. These are cardioselective receptors so you won’t find them elsewhere.
β2 receptors are in the lungs and smooth muscle of the vasculature. They increase bronchodilation and vasodilation.
β3 regulates catacholamine-induced thermogenesis. (Part of how we create heat)


What are common β-blockers?:

  • Atenolol (Tenormin)
  • Acebutolol (Sectral)
  • Metoprolol (Toprol)
  • Propanolol (Inderal)
  • Carteolol (Cartrol)
  • Timolol (opthalmic use)
  • Sotalol (Betapace)
  • Labetalol (Trandate)
  • Carvedilol (Coreg) (β1 and α1 receptor)

Be on the lookout for duplicate therapies!
Beta-Blockers are often administered orally, but are sometimes administered opthalmically or by nebulizer (β2 receptors are in the lungs, remember!). Patients who are on Coreg or Labetalol as well as another Beta-Blocker (usually metoprolol) have a higher likelihood of orthostasis.

Patients who utilize beta blockers typically do so immediately after a cardiac procedure or to regulate chronic atrial fibrillation (A-Fib). There are other abnormal heart rhythms that beta blockers can be used for, but A-Fib is the most common. If you have a patient who has had an ischemic stroke, you can bet money on them taking beta-blockers. Irregular heart rhythms like A-Fib increase risk of clot formation and, therefore, ischemic strokes.

So if we have a patient on beta blockers, what do we need to do?

Monitor for adverse events. With orthostasis being so risky for our older population and so common when present in addition to dehydration, you have to be on the look out for it all the time. We’ve talked about orthostasis before and identified it as a drop in blood pressure due to changes in position against gravity. Some days it may be present and some days it won’t be. So what do you do if you expect it? Well, you need to assess orthostatic vitals. The CDC has a basic assessment handout for this. I’ve added it here for you to download (see download below picture). (Source) It is part of the STEADI toolkit, if you are a geriatric provider and are familiar with that.

So here’s the rub. (Ha! Cardiac joke…) My patients tend to be very low level, acute or chronically ill, on many medications, and/or unable to safely stand due to hypotension. So, I ask my patient to transition from supine to seated FIRST, wait there for 1 minute while I take their blood pressure, and then progress to standing IF they are at least 90/60 or not terribly symptomatic. However, I cannot tell you how many times I haven’t been able to let someone stand because they’ve already dropped below 90/60 in sitting. Please, PLEASE add a seated phase to this assessment.

Educate patient on signs and symptoms of orthostasis so they know when they need to sit or perform some activity in seated prior to standing to increase their circulation and blood pressure prior to standing. And when you do exercise them, there are a few factors you need to be thinking about.

So why do patients with COVID-19 need beta-blockers?

Let’s remember some important things about COVID-19. It is a viral infection that, if it damages enough alveolar basement membranes and parenchymal cells, creates interstitial edema which results in ARDS. This damage is severe and requires some type of ventilatory assistance to sustain life. Some patients can recover from this as their bodies heal the damaged pneumocytes with either scar tissue (which doesn’t diffuse oxygen) or replacement parenchyma (if the basement membranes were not destroyed). Either way, they will be in a significantly oxygen-deficient state for some time.

We know that these patients don’t typically go home after ICU. Sometimes they go to sub-acute settings like rehab or skilled nursing, and other times they transition to home because it wouldn’t be safe for them to be in a group setting. But overall, they need more time to recover than what acute care, understandably, has to offer. “When COVID Comes Home” is something I’ve focused on here for over a month. This sub-acute time frame is now being recognized as the next “COVID nightmare”.

So when these patients come home or head to rehab in this deoxygenated state, they don’t magically get better with supplemental oxygen. They still have significant oxygen diffusion problems due to damaged lung tissue and we, as the rehab clinicians, are about to ask them to start working a bit harder. It is estimated at this point that this may las tup to two months after extubation.

Then we add some comorbidities into the mix. We know that people who have an already compromised cardiopulmonary system are more likely to contract COVID-19. Our patients with COPD, Diabetes, Heart Failure, history of AMI… the list goes on. These patients are already on beta blockers in addition to a host of other medications that also have effects on heart rate and blood pressure.

Why? Why is this the case? If you remember our talk in my post on pulse oximetry, I discussed how to tell the difference between deconditioning, orthostasis, and diffusion impairment based on vitals response to activity. When patients with diffusion impairments exercise, their O2 saturation drops. In an effort to compensate for this, the heart rate and blood pressure will rapidly rise and the patient will very quickly lose their exercise tolerance and/or cross the barrier into unsafe vitals response to exercise. We need to temper the quick desaturation with beta blockers to reduce cardiac oxygen demand so that the cardiac muscle tissue is less affected by ischemia. Beta-blockers are the answer to prevention of this entire compensatory response that will allow vitals to remain within tolerable range longer to support functional mobility, and eventually exercise and rehab.

What do I need to know for exercising these patients?

People who are on beta blockers experience a blunted heart rate response to exercise. What that means is that the beta blocker medication is working to decrease cardiac oxygen demand by decreasing heart rate. It will take your body longer (about 5 minutes, sometimes more) to overcome this mechanism and begin to elevate heart rate in response to exercise (aka increased oxygen demand). So you need a warmup. And not just a few stretches. You need a progressive warmup that slowly increases oxygen demand, ramping upward toward your target intensity of activity over the course of 5-10 minutes. This also means that, while you are exercising them, you cannot use heart rate as a measure of exertion. You have to use something else like an RPE scale of some sort, or maybe the RPD Scale.

What activities do you like to use to prevent orthostasis in your patients? Let me know in the comments!

More from the Pulmonary Rehab Toolbox…


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

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