Is checking for orthostatic hypotension less than 1 minute after standing clinically useful?

Not only can it be useful in identifying those with history of dizziness upon standing but it may also predict a higher risk of falls, fracture, syncope and mortality long term. 1

Clinicians (myself included) have often assumed that drops in blood pressure (BP) and brief feeling of light-headedness soon after active standing are too common and “physiologic” to be of clinical utility,1,2 and have often discouraged checking for orthostatic hyotension (OH) sooner than 1 minute.

However, a 2017 report involving over 11,000 middle-aged participants (Atherosclerosis Risk in Communities Study) may make us rethink our position. This prospective study  found a significant association between participant-reported history of dizziness on standing and OH (defined as a drop in BP systolic ≥20 mmHg or diastolic ≥10 mmHg) but only at 1st measurement (mean of 28.0 seconds after standing), not at subsequent ones over a 2 minute period.

The more intriguing finding was the association between OH documented < 1 minute after standing and increased risk of falls, fracture, syncope, and mortality over a median follow-up period of 23 years. Although there were limitations to the study (eg, excluding many patients likely to have more severe OH), it appears that “premature” checking for OH less than a minute after standing  may not be useless!

Most, including the CDC, agree that rechecking the BP at 3 minutes is still indicated to identify those with sustained or delayed OH. 2,3

Also go to a related P4P post: https://pearls4peers.com/2015/12/14/how-can-i-be-sure-that-my-patient-truly-has-orthostatic-hypotension-oh/

References

  1. Juraschek SP, Daya N, Rawlings AM, et al. Comparison of early versus late orthostatic hypotension assessment times in middle-age adults. JAMA Intern Med 2017;1177:1316-1323. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5661881/
  2. Singer W, Low PA. Early orthostatic hypotension and orthostatic intolerance-more than an observation or annoyance. JAMA Intern Med 2017;1177:1234-25. https://jamanetwork.com/journals/jamainternalmedicine/article-abstract/2645144
  3.  CDC. https://www.cdc.gov/steadi/pdf/measuring_orthostatic_blood_pressure-a.pdf. Accessed February 7, 2017.

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Is checking for orthostatic hypotension less than 1 minute after standing clinically useful?

How should I manage hypertension in my patient with neurogenic orthostatic hypotension?

The frequent concurrence of supine hypertension (SH) and neurogenic orthostatic hypotension (nOH)1 makes treatment of SH in these patients particularly challenging.

To begin with, your threshold for treatment of SH in patients with neurogenic orthostatic hypotension (nOH) may need to be higher than that commonly recommended by national guidelines for treatment of essential hypertension to avoid exacerbation of nOH.  Although SH in nOH patients is often arbitrarily defined as a systolic BP ≥150 mmHg or diastolic BP≥90 mmHg, a supine systolic BP of up to 160 mmHg may not warrant treatment, particularly if the symptoms of nOH have improved.2

A 2017 consensus panel recommends treatment of SH in the setting of nOH if systolic BP exceeds the range of 160-180 mmHg or diastolic BP exceeds 90-100 mmHg.  “Permissive” approach to SH in this setting may be reasonable, particularly in those with the largest drops in BP upon standing ( >80 mmHg drop). 2

Regardless, all patients with nOH and SH should be advised to avoid supine posture during the day and elevate the head of the bed as tolerated during the night.

If necessary, significant SH may be treated with short acting agents, including2:

  • Captopril 25 mg qhs
  • Clonidine 0.2 mg with evening meal
  • Hydralazine 10-25 mg qhs
  • Losartan 50 mg qhs
  • Nitroglyerine patch 0.1 mg/h patch qhs (remove patch in am)

Long acting antihypertensive agents and diuretics should be avoided given their inherent risk of significant exacerbation of nOH.

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References

  1. Goldstein DS, Pechnick S, Holmes C, et al. Association between supine hypertension and orthostatic hypotension in autonomic failure. Hypertension 2003; 42:136-142. https://www.ncbi.nlm.nih.gov/pubmed/12835329
  2. Gibbons CH, Schmidt P, Biaggioni I, et al. The recommendations of a concensus panel for the screening, diagnosis, and treatment of neurogenic orthostatic hypotension and associated supine hypertension. J Neurol 2017;264:1567-82. https://www.ncbi.nlm.nih.gov/pubmed/28050656
How should I manage hypertension in my patient with neurogenic orthostatic hypotension?

What pharmacological options should I consider when treating neurogenic orthostatic hypotension in my elderly patient with supine hypertension?

Treating symptomatic neurogenic orthostatic hypotension (nOH) in patients with supine hypertension can be challenging.

Before adding new agents, consider discontinuation or dose reduction of medications that can potentially aggravate orthostatic symptoms (eg, diuretics, vasodilators, negative chronotropic agents, including beta blockers).

Midodrine (an α1-adrenoreceptor agonist) and droxidopa (a norepinephrine pro-drug) are the only 2 FDA-approved drugs for the treatment of OH.

  • Midodrine is typically dosed between 2.5 mg-15 mg 1-3x/d during waking hours (prior to getting out of bed, before lunch, mid-afternoon).
  • Droxidopa is dosed from 100-600 mg 3x/day during waking hours (eg, 8 AM, noon, 4PM).
  • To reduce the risk of supine hypertension, these agents are not recommended to be taken within 5 h of bedtime, and should be used with caution in patients with congestive heart failure and chronic renal failure.

Fludrocortisone and pyridostigmine are used off-label for treatment of nOH.

  • Fludrocortisone (typical dose 0.1-0.2 mg/day) expands intravascular blood volume by increasing renal sodium and water reabsorption, with an attendant risk of exacerbating supine hypertension, hypokalemia, and edema.
  • Pyridostigmine (typical dose 30-60 mg 1-3x/day) is an acetylcholinesterase inhibitor that potentiates neurotransmission in the sympathetic ganglia and has the advantage of not worsening supine hypertension. Side effects include abdominal cramps, diarrhea, excessive sweating and urinary incontinence.

In practice,  1 or more of these agents are often used along with non-pharmacological measures.

Go to a related pearl at https://pearls4peers.com/2017/09/18/which-non-pharmacological-approaches-may-help-symptoms-of-orthostatic-hypotension-in-my-patient-with-autonomic-insufficiency/.

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Reference

Gibbons CH, Schmidt P, Biaggioni I, et al. The recommendations of a concensus panel for the screening, diagnosis, and treatment of neurogenic orthostatic hypotension and associated supine hypertension. J Neurol 2017;264:1567-82.https://www.ncbi.nlm.nih.gov/pubmed/28050656

 

What pharmacological options should I consider when treating neurogenic orthostatic hypotension in my elderly patient with supine hypertension?

Which non-pharmacological approaches may help symptoms of orthostatic hypotension in my patient with autonomic insufficiency?

A number of simple measures to help reduce the symptoms of neurogenic orthostatic hypotension (nOH) in susceptible patients have been recommended.1

  • Blood volume repletion (a minimum of 64 oz or 2L of water intake daily), depending on cardiac status. In addition, rapid consumption (within 5 min) of 16 oz or 500 ml of water can raise blood pressure by 30 mmHg for about an hour. It’s worth noting that liquids other than water (eg, water plus salt) do not provide the same BP response, likely due to water-induced hypo-osmolar reflex in the portal circulation.2,3
  • Increase salt intake if possible (eg, add 1-2 teaspoons or 2.3-4.6 g of salt per day), as many patients with nOH have an inadequate salt intake.
  • Improve physical conditioning that is not gravitationally challenging (eg, stationary recumbent bicyle, rowing machine).
  • Avoid increased core body temperature (eg hot tubs, prolonged hot showers).
  • Head-up position while sleeping through use of a wedge under the mattress or blocks under the head of the bed so that the head is 6-9 inches (15-23 cm) higher than the feet. This is to minimize nocturnal supine hypertension which can cause pressure diuresis and volume depletion.
  • Compressive garments, preferably either an abdominal binder or thigh high stockings when erect; knee high stocking are not likely to be effective.
  • Smaller, more frequent,  meals not high in carbohydrates in patients with postprandial hypotension.
  • Dietary supplementation with B12 or iron, if deficient.

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References

  1. Gibbons CH, Schmidt P, Biaggioni I, et al. The recommendations of a consensus panel for the screening, diagnosis, and treatment of neurogenic orthostatic hypotension and associated supine hypertension. J Neurol 2017;264:1567-1582. https://www.ncbi.nlm.nih.gov/pubmed/28050656
  2. Jordan J, Shannon JR, Black BK, et al. The pressor response to water drinking in humans: a sympathetic reflex? Circulation 101:504-9. http://circ.ahajournals.org/content/101/5/504.long
  3. Raj SR, Biaggioni I, Black BK, et al. Sodium paradoxically reduces the gastropressor response in patients with orthostatic hypotension. Hypertension 2007;48:329-334. https://www.ncbi.nlm.nih.gov/pubmed/16785332
Which non-pharmacological approaches may help symptoms of orthostatic hypotension in my patient with autonomic insufficiency?

How can I be sure that my patient truly has orthostatic hypotension (OH)?

OH is a sustained reduction of systolic blood pressure (SBP) of ≥ 20 mm Hg or diastolic BP ≥ 10 mm Hg within 3 min of standing or head-up tilt to at least 60° on a tilt table (1); symptoms are not part of the criteria. In patients with supine hypertension, a reduction in SBP of 30 mm Hg has been suggested (1).  

The Centers for Disease Control and Prevention (CDC) recommends BP measurements when patient is supine for 5 min, and after standing for 1 and 3 min (2).  In some patients symptomatic OH occurs beyond 3 minutes of standing (1). Preference for mercury column sphygmomanometer due to its reliability and simplicity, with arm at the level of the heart has been stressed (3). 

A 2017 report involving over 11,000 middle-aged participants (Atherosclerosis Risk in Communities Study) has challenged the notion of waiting 3 minutes before OH is measured (4).  This prospective study  found a significant association between participant-reported history of dizziness on standing and OH but only at 1st measurement (mean of 28.0 seconds after standing), not at subsequent ones over a 2 minute period. It was concluded that measuring OH during the first minute “not only makes a lot of sense” but it’s more appropriate “because it’s more predictive of future falls”.

Keep in mind that OH is more common and more severe during mornings and after meals, and is exacerbated by large meals, meals high in carbohydrate, and alcohol intake (1).

For a relate pearl go to : https://pearls4peers.com/2018/02/08/is-checking-for-orthostatic-hypotension-less-than-1-minute-after-standing-clinically-useful

References

  1. Freeman R, Wieling W, Axelrod FB, et al. Consensus statement on the definition of orthostatic hypotension, neurally mediated syncope and the postural tachycardia syndrome. Autonomic Neuroscience: Basic and Clinical 2011;161: 46–48. https://www.ncbi.nlm.nih.gov/pubmed/21431947
  2. http://www.cdc.gov/steadi/pdf/measuring_orthostatic_blood_pressure-a.pdf , accessed Dec 13, 2015.
  3. Naschitz J, Rosner I. Orthostatic hypotension: framework of the syndrome . Postgrad Med J 2007; 83:568-574. http://pmj.bmj.com/content/83/983/568
  4. Juraschek SP, Daya N, Rawlings AM, et al. Comparison of early versus late orthostatic hypotension assessment times in middle-age adults. JAMA Intern Med 2017;1177:1316-1323. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5661881/

 

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How can I be sure that my patient truly has orthostatic hypotension (OH)?