beta blockers and POTS…

Beta blockers are one of the most popular and first-prescribed treatments for postural orthostatic tachycardia syndrome (POTS) because they help treat tachycardia by lowering heart rate. But how exactly do they work?

Throughout your sympathetic nervous system (the fight-or-flight portion of your nervous system) are receptors for epinephrine and norepinephrine called adrenergic receptors. There are several subtypes of adrenergic receptors, including some which, when stimulated, result in increased cardiac activity. These receptors are called beta receptors, or beta adrenergic receptors.

There are three types of beta adrenergic receptors:

• Beta-1 receptors are primarily located in cardiac tissue. When stimulated, these receptors cause an increase in heart rate, blood pressure, and cardiac contraction.
• Beta-2 receptors are primarily found in smooth muscle of the body, especially surrounding the airways and lungs. When stimulated, the bronchioles dilate to promote the flow of oxygen.
• Beta-3 receptors are primarily found in fat cells and are not relevant for our current discussion.

As part of the sympathetic nervous system, the receptors prepare to “fight” or “flight” through increased oxygenation and cardiac output when they are stimulated by epinephrine and norepinephrine. Beta blockers block epinephrine and norepinephrine from binding to beta receptors, helping to reduce the fight-or-flight response.

Generally, beta blockers target both beta-1 and beta-2 receptors to block the effects of epinephrine and norepinephrine. As you might expect, blocking the stimulation of beta-1 and beta-2 receptors results in an opposite reaction to the stimulation. Thus, instead of increasing heart rate and blood pressure, blocking beta-1 receptors causes a decrease in both. And, instead of dilating the bronchioles, blocking beta-2 receptors constricts bronchioles. This can cause issues for people who have asthma, COPD, or other airway construction.

To address this unwanted effect for people with airway constriction that need a beta blocker for arrhythmia, high blood pressure, or heart disease, drug manufacturers eventually developed another type of beta blocker. This type is “cardioselective”, meaning it blocks stimulation of the cardiac beta receptors.

Cardioselective beta blockers primarily target beta-1 receptors, although in high doses may also target beta-2 receptors, and thus work by reducing heart rate and blood pressure without causing airway constriction. Non-cardioselective beta blockers target both beta-1 and beta-2 receptors and therefore are not recommended for people with asthma, COPD, airway constriction or other breathing difficulties.

The following is a list of some popular cardioselective and non-cardioselective beta blockers:

In addition to lowering heart rate, beta blockers also lower blood pressure. For those with POTS and hypotension, beta blockers may not be the best treatment. At the very least, blood pressure and heart rate should be monitored while undergoing beta blocker therapy to ensure neither are dropping too low.

Other side effects of beta blockers include:

• Dizziness.
• Weakness.
• Drowsiness or fatigue.
• Cold hands and feet.
• Dry mouth, skin, or eyes.
• Headache.
• Upset stomach.
• Diarrhea or constipation.

Know what a lot of those sound like? POTS. So, if you take this medication to help relieve your POTS symptoms, it could – wait for it – give you POTS symptoms. In a previous post I also discussed that beta blockers can cause non-allergic rhinitis, which can be bothersome for those of us who already suffer from rhinitis.

So, if you take a beta blocker, or if your doctor has mentioned prescribing it, be sure to discuss with your doctor if you have:

• hypotension (low blood pressure),
• asthma, COPD or other airway constriction,
• sinus or allergy issues, or
• bradycardia (low heart rate).

As you may remember, I am on atenolol (cardioselective) and have been for almost 7 years. Over that time, I have developed a sort of attachment to atenolol. It does an excellent job of controlling my heart rate, but over the years I have had to decrease to a smaller and smaller dose as atenolol began to cause hypotension and bradycardia. The lowest HR I have ever seen is 39bpm, the lowest I have ever recorded while sleeping is 36.

A typical starting dose of atenolol for someone who takes it for on-label use is 50 mg. I take a 25mg pill (the smallest available), and cut it into quarters. So, I take approximately 6 mg. I can’t cut it any smaller without the pill crumbling. Last week at my cardiologist appointment my blood pressure was 86/40, which isn’t totally abnormal these days. So, yeah, I still need a smaller dose.

Because atenolol can’t be compounded and 25mg is the smallest dose available, my cardiologist wants to try a new beta blocker, but it’s non-cardioselective. Nadolol can be compounded so that my starting dose will be 4mg, and I can have it compounded smaller, if necessary. I had asthma as a child, but have no reason to think that would have any effect, especially at such a small dose.

I have reached a point where I can handle the tachycardia without a beta blocker, the only reason I continue to take it is because I can’t handle the adrenaline. I need something that controls the adrenaline without causing the side effects of controlled adrenaline. So if you could get right on that…

“All truths begin as blasphemies.” – George Bernard Shaw

Smell ya later.
– Linds