Symptomatic Orthostatic Hypotension Complicating the Management of Chronic Hypertension: A Vexing Clinical Problem With No Easy Solutions

Michael J. Bloch, MD
Associate Professor, University of Nevada School of Medicine
Medical Director, Vascular Care, Renown Institute for Heart and Vascular Health
President, Blue Spruce Medical Consultants, PLLC
Reno, Nevada

Bloch MJ. Symptomatic Orthostatic Hypotension Complicating the Management of Chronic Hypertension: A Vexing Clinical Problem With No Easy Solutions. Consultant360. Published online  November 2, 2022.


Maintenance of cerebral perfusion when moving from a seated or supine position to an upright position is a complicated physiological process, whereby the carotid baroreceptor, sensing decreased stretch, inhibits the parasympathetic nervous system and activates the sympathetic nervous system (SNS), leading to increased heart rate, venoconstriction, and increased arterial resistance. While the SNS is the primary driver in this process, volume status and level of activation of the renin-angiotensin-aldosterone system also play a role, particularly in patients with impaired baroreceptor function.

Orthostatic hypotension (OH) is defined as a decrease in systolic blood pressure (BP) of at least 20 mmHg or diastolic BP of at least 10 mmHg within 1 to 3 minutes of standing.1  While this arbitrary definition is helpful in making the diagnosis, it is important to realize that a patient’s symptoms while standing may not correlate with the magnitude of BP reduction, and some patients may develop symptoms at shorter or more delayed intervals. Symptoms can also occur with drops in BP that do not reach a truly hypotensive range. As described in a strong review article and accompanying editorial, OH is a frequent problem that should be controlled in patients who are treated for hypertension. And although there are a paucity of high-quality data to aid decision-making, a rational approach to diagnosis and treatment is presented therein and summarized in this article.2,3

Patients who are treated for hypertension are at an increased risk of OH due to a variety of mechanisms, including the assumptions that: 1) chronic hypertension and OH may both arise from abnormal BP regulatory mechanisms; 2) pharmacologic treatment of hypertension may worsen OH; 3) certain clinical characteristics such as a history of cardiovascular events, diabetes, or chronic kidney disease are common contributors to both conditions; and 4) cerebral autoregulation and vasoreactivity may be impaired in patients with chronic hypertension. Often overlooked due to increased pressure naturesis, supine hypertension, particularly at night, or poorly controlled hypertension are also important contributors to OH. While landmark clinical trials like the Systolic BP Intervention Trial (SPRINT) and Action to Control Cardiovascular Risk in Diabetes (ACCORD) have not demonstrated vastly increased risk of OH with more aggressive BP treatment, patients with severe OH at baseline were not likely included.4,5

In the absence of symptoms, there is little consensus about whether the presence of OH should lead to changes in hypertension management. Lightheadedness or other symptoms provoked by standing are relatively common and not specific to the disorder; thus, the first step in management is trying to link symptoms to documented orthostatic changes. This is primarily accomplished through measuring BP in multiple positions, either in or out of the office, and attempting to correlate the BP changes with symptoms. In patients whose symptoms do not appear to correlate with BP changes, etiologies other than OH—benign positional vertigo, postural orthostatic tachycardia, and post-prandial hypotension, for example—should be investigated. In patients with suspected or confirmed OH, the next step is identifying and correcting any compounding or underlying conditions, including volume depletion, adrenal insufficiency, anemia, deconditioning, heart failure, valvular heart disease, arrythmia, Parkinson disease, Lewy body dementia, multiple system atrophy, pure autonomic failure, diabetes neuropathy, amyloidosis, vitamin b12 deficiency, or use of alcohol, sedatives, antidepressants, or other prescription or over the counter medications that may lead to relative hypotension or interfere with the SNS.

Nonpharmacologic interventions for patients with OH have not been well-validated. Countermeasures, such as leg crossing when standing or use of abdominal binders, are frequently recommended, but there are a paucity of data demonstrating their value. Since it reduces supine hypertension and resulting pressure natriuresis, elevating the head of the bed is probably helpful in improving early morning volume status and decreasing symptoms upon first getting up from bed. Increased sodium and water intake is frequently recommended, but since it can lead to increased supine hypertension and pressure natriuresis, it may be counterproductive.

Adjusting one’s antihypertensive medications may be beneficial. In general, agents that block the SNS, including beta-blockers and peripheral alpha blockers, should be avoided. Diuretics may increase the risk of symptoms but can be used in caution when needed to control supine hypertension. Dihydropyridine calcium channel blockers, angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers are preferred agents. Occasionally, it may be useful to employ short-acting hypertensives before bedtime, but patients should be monitored for early morning hypotension. It may be reasonable to liberalize BP goals in patients with OH, but this needs to be carefully balanced with the effects on cardiovascular risk and supine pressure natriuresis.

In patients whose symptoms persist despite these interventions, pharmacologic approaches to treating OH include the use of mineralocorticoid fludrocortisone, the alpha-1 agonist midodrine, or the norepinephrine precursor droxidopa, but they can each lead to increased supine BP and perhaps cardiovascular risk. The cholinesterase inhibitor pyridostigmine may also offer modest improvement in standing BP without significantly increasing supine BP.

Symptomatic OH can be a vexing barrier to BP control, particularly in older adults or those with established neurodegenerative or cardiovascular disease. Once the diagnosis is made, careful consideration needs to be given to identifying and, if possible, treating contributing conditions. Pharmacological management of OH requires a nuanced approach to determining seated BP goals and adjusting medications.


  1. Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Hypertension. 2018;71(6):e13. doi:10.1161/hyp.0000000000000065
  2. Raber I, Belanger MJ, Farahmand R, et al. Orthostatic hypotension in hypertensive adults: Harry Goldblatt award for early career investigators 2021. Hypertension. 2022;79:2388-2396. doi:10.1161/HYPERTENSIONAHA.122.18557
  3. Juraschek SP, Biaggioni I. Management of patients with hypertension and orthostatic hypotension: parallel progress. Hypertension. 2022;79:2385-2387. doi: 10.1161/HYPERTENSIONAHA.122.19113
  4. Fieg JL, Evans GW, Marolis KL. Orthostatic hypotension in the ACCORD (action to control cardiovascular risk in diabetes) blood pressure trial: prevalence, incidence, and prognostic significance. Hypertension. 2016;68(4):888-895. doi:10.1161/HYPERTENSIONAHA.116.07474
  5. Juracschek SP, Taylor AA, Wright JT, et al. Orthostatic hypotension, cardiovascular outcomes and adverse events: results from SPRINT. Hypertension. 2020;75(3):660-667. doi: 10.1161/HYPERTENSIONAHA.119.14309