Orthostatic hypertension and strokes

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That’s right you read the title correctly- it reads orthostatic hypertension and not hypotension.  Ordering orthostatics on patients is quite common.   Most of the time the clinical query is in regards to the latter (hypotension).  My mentor, Dr. Andreoli, would often refer to performing orthostatics in the hospital as the “death provocation test”.  He reasoned that a great majority of hospitalized patients with acute illness will have a significant drop in blood pressure after rising from a seated position.  He felt this was likely not always indicative of volume depletion, but rather from a global sympathetectomy from their acute illness.  If we asked a patient to quickly rise and they did in fact have a robust drop in blood pressure a topple to the floor with resulting head trauma could occur.  Always makes me want to have a couple of extra hands on deck when performing this maneuver.  But, what about performing orthostatic blood pressure measurements on stable outpatients with no complaints. 
I read an interesting editorial in Hypertension this week in regards to orthostatic hypertension.  It took a few glances to read that correctly.  Occasionally I check orthostatic blood pressures on patients in the clinic and get a surprising result.  A huge increase in blood pressure of 40 mmHg from sitting to standing.  I never really thought about the long term consequences of this until I read this editorial and accompanying article by Yatsuya et al.  
Yatsuya et al. prospectively followed 12,817 patients (in the ARIC study) who had baseline orthostatic blood pressure measurements.  They further grouped theses patient into several baseline categories depending on their BP changes from sitting to 2 min after standing.

  1. Decline in BP- Major (-63 to -20), 547 subjects or Minor (-20 to -10), 1507 subjects 
  2. Stable BP- (-10 to +10), 8981 subjects 
  3. Increase in BP- Major (+65 to +20), 303 subjects or Minor (+20 to +10), 1479 subjects

Data was obtained in regards to ischemic stroke incidence and type for a median of 18.7 years.  They report:

  • Little change in BP after standing in the entire cohort.  SBP increased 0.4 mmHg and DBP increased by 3mmHg. 
  • Patients with orthostatic SBP and DBP decreases of greater than 20mmHg had an increased incidence of thrombotic and cardioembolic strokes. 
  • Patients with orthostatic SBP decreases and increases of greater than 20mmHg had an increased incidence of lacunar strokes.  

The authors conclude that these findings are consistent with previous studies showing silent strokes in elderly hypertensive patients with orthostatic hypo- or hypertension.  They speculate that this BP elevation from sitting to standing could be due to excessive sympathetic nervous system activation, which could in turn lead to endothelial dysfunction.  Another theory discussed in the editorial and by these authors is that elderly patients with orthostatic hypertension have been shown have excessive BP dipping at night with greater than a 25mmHg drop in BP (referred to as “extreme dipping“).  These “extreme dippers” had an increased risk of silent stroke as well.  Several limitations are present.  Only a baseline orthostatic value is present.  How would these values change over time or would they hold true?  Second, not every participant had an MRI to look for silent strokes.  However, this study was prospective and contains a large sample size.  

How will this change practice? Hard to say.  This could merely serve as a marker for autonomic dysfunction and might not be a modifiable risk factor.  Simple measures such as compression stockings have been used to control both orthostatic hypo- and hypertension.  Beta blockers could be useful in controlling orthostatic hypertension.  Further clinical trials to directly examine these relationships could help in answering these questions.


  1. I am a physician with ADPKD. I have orthostatic hypertension and during the course of a day may need to be treated for hypertension and hypertension. Staying in bed seems to be the only way to control my BP but that is not a reasonable solution. I have tried Verapamil regular formulation but still sometimes get hypotension even with just one 80 mg tablet per day.
    where is a good place to get a comprehensive workup for this problem? I have read about the center at Vanderbilt but it seems to focus on orthosatic hypertension related to POTS.
    Thanks for any assistance.

  2. I am a physician with ADPKD. I have been taking Amlodipine and Verapamil but have a problem with orthostatic hypertension. When I take Verapamil for BP control I often time will experience hypotension upon lying down.
    Where can I get a comprehensive work up for this bedeviling problem. I feel like I am caught between the devil and the deep blue sea.

  3. Maybe related. My blood pressure DROPS when I sit or lay down. I'm assuming my legs are maintaining the blood pressure while in the vertical position.

    Due to lymphoma I had several servings of CHOP, ICE and then Stem Cell Transplant.

    My difficulties seem to be a combination of peripheral nerve damage and Brain damage (cns).

    I take Dexedrine extended release which helps a Lot during the day but not perfect. In the evenings I have to lay down often.

  4. I Seem to be one of those "dippers" you refer about. When i go from a sit to standing postion within a min or 2 my blood pressure will shoot up from 130/80 to 210/110 was the heighest recorded. and that was after 20 mins of sitting. In the evening it drops down the lowest has been 98/64. The Hypo in the past few days and the hyper for around 6 months. That i started feeling it anyways.

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