I recently had a short stay in the hospital for low blood pressure and a slow heart rate(also called Bradycardia). I had a few EKG's, an Echocardiogram, and a Stress Test. The doctors took me off of my beta blocker that I have been on for years. When my blood pressure leveled out, they sent me home.
My doctor was out of town at the time and not expected to be back for a few weeks. A few days after I got home, I started having dizzy spells (Syncope). So, I started checking my blood pressure and it was high. I decided I didn't want to go back to the hospital and would wait it out and see what my doctor said when she got back. Since I had gone from really low BP and heart rate to having high BP and HR, I decided to look up how to do a "Poor Man's Tilt Table Test". You can read more on how to do this here. And there is a link to the right on what a tilt table test is.
I had some help doing it, but we did three of them. All three of them caused my BP and HR to raise over the requisite 30 beats above the resting BP and HR.
I knew what Orthostatic Hypotension was. It is sometimes also called Neurally Mediated Hypotension.But with it, your blood pressure drops 25 mmHg, without the increase in HR that I was having. When my husband was diagnosed, they didn't separate out Orthostatic Hypotension from POTS. And depending on who was talking to us, they were using the two terms interchangeably. Now they are two distinct diagnoses, although you can have both.
I was pretty concerned because I had never heard of BP going up to the degree mine was when I stood up. So, I did a google search.
I found out that there is a subclass of orthostatic intolerance that causes this called ORTHOSTATIC HYPERTENSION. This is what I could find out about it. There wasn't much information available.
In general, it is simply when your BP rises upon standing. Orthostatic hypertension was defined as either an increase in DBP (diastolic) from <90 mmHg to ≥90 mmHg or an increase in SBP(systolic) from <140 mmHg to ≥140 mmHg.
Studies have shown that people who have Mast Cell Activation Syndrome and POTS sometimes have Orthostatic Hypertension. People with baroreflex failure also have bouts of it. Another rare condition called norepinephrine transporter deficiency can also cause this increase in blood pressure on standing. And pheochromocytoma can also cause it. And finally, diabetes can cause it. Diabetics are prone to having neuropathy (nerve damage), and it is likely that neuropathy has some connection to Orthostatic Hypertension.
Patients usually have venous pooling in the lower legs. This means that a large amount of blood collects in your lower legs when you stand up. This causes a decrease in the cardiac output of your heart. That in turn, causes your sympathetic nervous system to become activated. And then your arteries become severely constricted. This is similar to the POTS occurs. POTS happens because of dysautonomia in the lower legs which results in venous pooling. But the difference is that POTS patients don't always have symptoms of Orthostatic Hypertension.
Different studies have used different criteria for diagnosing Orthostatic Hypertension.
One study used the following: ≥20 mmHg increase in SBP upon assuming an upright posture ( head-up tilting to 70 degrees) from the supine position.
Generally, this result needs to be reproducible because people with conditions like essential hypertension (regular high blood pressure) or diabetes have more variation in blood pressure readings than otherwise healthy people.
Aside from the rise in BP when you stand there are other tests that need to be run in order to diagnose underlying causes. Your doctors need to know if there is something that needs to be corrected with surgery, or if you have baroflex failure.
To treat it, the most obvious line of treatment is to treat your high blood pressure, if you have it. Activation of the sympathetic nervous system should be controlled with things like alpha-1 adrenergic receptor antagonists such as prazosin, or central alpha-2 adrenergic receptor agonists such as clonidine.
More on this subject can be found here: Orthostatic Hypertension: When Pressor Reflexes Overcompensate
My doctor was out of town at the time and not expected to be back for a few weeks. A few days after I got home, I started having dizzy spells (Syncope). So, I started checking my blood pressure and it was high. I decided I didn't want to go back to the hospital and would wait it out and see what my doctor said when she got back. Since I had gone from really low BP and heart rate to having high BP and HR, I decided to look up how to do a "Poor Man's Tilt Table Test". You can read more on how to do this here. And there is a link to the right on what a tilt table test is.
I had some help doing it, but we did three of them. All three of them caused my BP and HR to raise over the requisite 30 beats above the resting BP and HR.
I knew what Orthostatic Hypotension was. It is sometimes also called Neurally Mediated Hypotension.But with it, your blood pressure drops 25 mmHg, without the increase in HR that I was having. When my husband was diagnosed, they didn't separate out Orthostatic Hypotension from POTS. And depending on who was talking to us, they were using the two terms interchangeably. Now they are two distinct diagnoses, although you can have both.
I was pretty concerned because I had never heard of BP going up to the degree mine was when I stood up. So, I did a google search.
I found out that there is a subclass of orthostatic intolerance that causes this called ORTHOSTATIC HYPERTENSION. This is what I could find out about it. There wasn't much information available.
In general, it is simply when your BP rises upon standing. Orthostatic hypertension was defined as either an increase in DBP (diastolic) from <90 mmHg to ≥90 mmHg or an increase in SBP(systolic) from <140 mmHg to ≥140 mmHg.
Studies have shown that people who have Mast Cell Activation Syndrome and POTS sometimes have Orthostatic Hypertension. People with baroreflex failure also have bouts of it. Another rare condition called norepinephrine transporter deficiency can also cause this increase in blood pressure on standing. And pheochromocytoma can also cause it. And finally, diabetes can cause it. Diabetics are prone to having neuropathy (nerve damage), and it is likely that neuropathy has some connection to Orthostatic Hypertension.
Patients usually have venous pooling in the lower legs. This means that a large amount of blood collects in your lower legs when you stand up. This causes a decrease in the cardiac output of your heart. That in turn, causes your sympathetic nervous system to become activated. And then your arteries become severely constricted. This is similar to the POTS occurs. POTS happens because of dysautonomia in the lower legs which results in venous pooling. But the difference is that POTS patients don't always have symptoms of Orthostatic Hypertension.
Different studies have used different criteria for diagnosing Orthostatic Hypertension.
One study used the following: ≥20 mmHg increase in SBP upon assuming an upright posture ( head-up tilting to 70 degrees) from the supine position.
Generally, this result needs to be reproducible because people with conditions like essential hypertension (regular high blood pressure) or diabetes have more variation in blood pressure readings than otherwise healthy people.
Aside from the rise in BP when you stand there are other tests that need to be run in order to diagnose underlying causes. Your doctors need to know if there is something that needs to be corrected with surgery, or if you have baroflex failure.
To treat it, the most obvious line of treatment is to treat your high blood pressure, if you have it. Activation of the sympathetic nervous system should be controlled with things like alpha-1 adrenergic receptor antagonists such as prazosin, or central alpha-2 adrenergic receptor agonists such as clonidine.
More on this subject can be found here: Orthostatic Hypertension: When Pressor Reflexes Overcompensate
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