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Orthostasis

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Last Update: January 13, 2019.

Introduction

Orthostasis, from the Greek orthos (upright) and histanai (to stand), is a normal physiological response of the sympathetic system to counteract a fall in blood pressure when a person is laying down and assumes the upright position. This compensatory response of the autonomic nervous system reveals the evolutionary adaptation of the human being to meet the needs of an erect posture, a unique characteristic that distinguishes humans from other species.

Physiology

When one stands up, gravity causes a shift of 500 to 800 mL of blood volume from the upper body to the lower body and the splanchnic circulation. This redistribution of blood decreases the venous return and the right atrium’s pressure, reducing the stroke volume and eventually a fall in arterial blood pressure.[1]

For this change in position, the body has 4 compensatory mechanisms:

  • Irregular distribution of blood in the venous system (there are pools of blood located in the central circulation, that can be used when hypotension is detected)
  • Non-uniform distensibility (small vessels are more rigid than large vessels. Thus, small veins prevent a large accumulation of blood in the lower body and help to maintain a relative upward flow of blood)
  • Muscle pumps (increase the venous return)
  • Autonomic reflexes

Out of these, autonomic reflexes are the most important mechanism.[2]

There are baroreceptors in the carotid sinus and in the aortic arch which play an important role in regulating blood pressure by sensing the grade of distension of the vessels. When there is a fall in blood pressure, tension on the vessel walls decreases and the afferent baroreceptor nerves decrease their firing rate to the medullary cardiovascular center (nucleus tractus solitarii in the medulla). This synapsis will inhibit the parasympathetic response (vagal) and stimulate the sympathetic response, causing generalized vasoconstriction, increased heart rate, and contractility. Baroreceptor activation also causes the activation of the renin-angiotensin-aldosterone system and the release of vasopressin by the pituitary gland. It results in sodium and water reabsorption by the kidney, increasing the plasma volume, and arterial vasoconstriction through angiotensin II type 1 receptor and V1 receptors in arterial blood vessels. Normally, an adequate response increases heart rate by 10 to 15 bpm, maintains the systolic pressure and elevates the diastolic pressure about 10 mm Hg.[3]

Pulmonary baroreceptors and atrial low-pressure baroreceptors play a small response, causing renal vasoconstriction the last one, with no significant contribution to increasing the blood pressure.

Clinical Relevance

When the autonomic compensatory mechanism is affected, there is a significant decrease of the central blood pressure, and symptoms of hypoperfusion can appear, e.g., dizziness, lightheadedness or syncope. This is called orthostatic hypotension.

Orthostatic hypotension (OH) is a clinical finding defined by a fall in systolic blood pressure over 20 mmHg or a fall of in diastolic pressure over 10 mm Hg within 3 minutes of standing.[4] Symptoms may be present, or it can be asymptomatic as well.

Etiology

Two principal conditions can lead to orthostatic hypotension: intravascular volume depletion and abnormal autonomic reflexes. Multiple disorders can cause an abnormal autonomic response, but about a third of patients with OH have no identifiable cause.[5] Neurogenic OH is the most common identifiable cause. A simple classification of the etiology divides it in acute (mostly symptomatic) and chronic (majority asymptomatic)[6][7]:

  • Acute-Nonneurogenic: dehydration, medications, adrenal insufficiency, infection, myocardial infarction
  • Chronic-Neurogenic: (Central) brain steam lesions, Parkinson disease, Lewy body dementia; (Peripheral) pure autonomic failure, diabetic neuropathy

Predisposing factors: Dehydration, deconditioning, malnutrition and aging. Medications associated with OH are antihypertensives, diuretics, vasodilators, antipsychotics, ethanol, opiates, and antidepressants.

Epidemiology

Orthostatic hypotension occurs more frequently in the elderly, and there is a proportional increase in advancing age. This could be explained due to arterial stiffness and reductions in baroreceptor reflex sensitivity, muscle pump activity, and alpha 1 adrenergic vasoconstriction.[8] In one large cross-sectional study (Rutan et al.) studied a population age 65 years or older to determine the overall prevalence of OH, the total prevalence was 18.2%, with only 2% being symptomatic.[9]

History and Physical

Orthostasis per se is asymptomatic, but symptoms may be present when there is orthostatic hypotension.

Symptoms of OH result from transient insufficient perfusion to organ tissue, mostly the brain. Dizziness, lightheadedness, weakness, blurred vision and in severe cases syncope, are the most commonly reported symptoms.[10] Another frequent symptom, but difficult to recognize is the so-called “coat-hanger” a discomfort or ache affecting the muscles of the back and nape neck that radiates to the occipital area of the skull. Due to neck muscles hypoperfusion.[11] Even though far less frequently, supine hypertension, erratic swings in blood pressure, angina, and stroke are manifestations of OH.[12]

Evaluation

The initial evaluation of OH must include measuring blood pressure, and heart rate after the patient has been recumbent for at least 5 minutes and again after 1 minute and 3 minutes of standing. The diagnosis is made with one or both criteria of the definition of orthostatic hypotension. For those patients with hypertension, a reduction of systolic BP of 30 mm Hg is more appropriate to define OH.[4]

A complete medical history and physical examination should be performed. With special regard to medications, comorbidities, potential volume losses, and a complete neurologic examination. Seeking clinical clues to possible etiologies.[8] The direction of the evaluation, laboratory, imaging and autonomic studies, should be guided by first differentiating acute or chronic causes.

The heart rate response is useful to give us a clue in the etiology. If the heart rate response to postural change is less than 15 bpm suggests a neurogenic OH. On the other hand, if there is an increase in heart rate of over 20 bpm suggests volume depletion or over 30 bpm suggests postural tachycardia syndrome. Postural tachycardia syndrome is another form of chronic orthostatic intolerance, mostly affecting children and young adults. These patients usually present the typical symptoms of orthostatic hypotension, but not meet the criteria for OH (little or no fall of blood pressure) and the autonomic response is associated with an exaggerated tachycardia.[13]

If there is a high suspicion of OH of neurologic origin, patients should be referred to an Autonomic Center for further evaluation. Although, regardless of the cause, the treatment of orthostatic hypotension is symptomatic.

Treatment / Management

The principal goal of the treatment in OH is to reduce adverse outcomes such as falls, disability, and impaired quality of life. Treatment is only indicated for those symptomatic and therapy should be driven by symptoms and not by targets of blood pressure.[14]

First, eliminate predisposing factors, especially medications, and exclude hypovolemic status. Then, start stepwise with non-pharmacological maneuvers, followed by pharmacologic interventions. Symptoms must be assessed in every consult to monitor progress.

  • Non-pharmacological therapy, the principal basis is to decrease venous pooling to the lower body, and to increase the intravascular volume: Physical maneuvers: change of position gradually, compression waist high stocking (30 to 40 mm Hg), avoid standing motionless, tensing leg muscles, an abdominal binder and exercise (swimming or recumbent biking). Lifestyle modification: increase salt consumption 6 to 10 grams per day and water intake 2 to 3 liters per day.[14]
  • Pharmacological therapy, the aim is to raise the blood pressure when the patient will stand up or will perform any activity in the upright position, avoiding side effects and the complications of increasing the blood pressure for a prolonged time. Fludrocortisone is the first-line treatment in the non-hypertensive patient. Second-line therapy includes midodrine indicated for patients with or without hypertension.[15] Other therapies include caffeine, pyridostigmine, erythropoietin, vasopressin analogues, yohimbine, among others.

Enhancing Healthcare Team Outcomes

Orthostasis is a relatively common problem in clinical medicine and is best managed by a multidisciplinary team because of the numerous causes. The key is to improve the quality of life with proper treatment.  First, eliminate predisposing factors, especially medications, and exclude hypovolemic status. Then, start stepwise with non-pharmacological maneuvers, followed by pharmacologic interventions. Symptoms must be assessed in every consult to monitor progress. Initially the treatment is non-pharmacological but for those who fail to respond, pharmacological therapy is the next step. The outlook for those who remain compliant with therapt are excellent.

Questions

To access free multiple choice questions on this topic, click here.

References

1.
Smit AA, Halliwill JR, Low PA, Wieling W. Pathophysiological basis of orthostatic hypotension in autonomic failure. J. Physiol. (Lond.). 1999 Aug 15;519 Pt 1:1-10. [PMC free article: PMC2269496] [PubMed: 10432334]
2.
Stewart JM. Mechanisms of sympathetic regulation in orthostatic intolerance. J. Appl. Physiol. 2012 Nov;113(10):1659-68. [PMC free article: PMC3524660] [PubMed: 22678960]
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Sahni M, Lowenthal DT, Meuleman J. A clinical, physiology and pharmacology evaluation of orthostatic hypotension in the elderly. Int Urol Nephrol. 2005;37(3):669-74. [PubMed: 16307360]
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Chisholm P, Anpalahan M. Orthostatic hypotension: pathophysiology, assessment, treatment and the paradox of supine hypertension. Intern Med J. 2017 Apr;47(4):370-379. [PubMed: 27389479]
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Arnold AC, Raj SR. Orthostatic Hypotension: A Practical Approach to Investigation and Management. Can J Cardiol. 2017 Dec;33(12):1725-1728. [PMC free article: PMC5693784] [PubMed: 28807522]
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Rutan GH, Hermanson B, Bild DE, Kittner SJ, LaBaw F, Tell GS. Orthostatic hypotension in older adults. The Cardiovascular Health Study. CHS Collaborative Research Group. Hypertension. 1992 Jun;19(6 Pt 1):508-19. [PubMed: 1592445]
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Raj SR. Postural tachycardia syndrome (POTS). Circulation. 2013 Jun 11;127(23):2336-42. [PMC free article: PMC3756553] [PubMed: 23753844]
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Miller ER, Appel LJ. High prevalence but uncertain clinical significance of orthostatic hypotension without symptoms. Circulation. 2014 Nov 11;130(20):1772-4. [PMC free article: PMC4888076] [PubMed: 25278100]
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Shibao C, Lipsitz LA, Biaggioni I. ASH position paper: evaluation and treatment of orthostatic hypotension. J Clin Hypertens (Greenwich). 2013 Mar;15(3):147-53. [PubMed: 23458585]
10.
Freeman R, Wieling W, Axelrod FB, Benditt DG, Benarroch E, Biaggioni I, Cheshire WP, Chelimsky T, Cortelli P, Gibbons CH, Goldstein DS, Hainsworth R, Hilz MJ, Jacob G, Kaufmann H, Jordan J, Lipsitz LA, Levine BD, Low PA, Mathias C, Raj SR, Robertson D, Sandroni P, Schatz I, Schondorff R, Stewart JM, van Dijk JG. Consensus statement on the definition of orthostatic hypotension, neurally mediated syncope and the postural tachycardia syndrome. Clin. Auton. Res. 2011 Apr;21(2):69-72. [PubMed: 21431947]
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Robertson D, Robertson RM. Causes of chronic orthostatic hypotension. Arch. Intern. Med. 1994 Jul 25;154(14):1620-4. [PubMed: 8031210]
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Gupta V, Lipsitz LA. Orthostatic hypotension in the elderly: diagnosis and treatment. Am. J. Med. 2007 Oct;120(10):841-7. [PubMed: 17904451]
13.
Grubb BP, Kosinski DJ, Kanjwal Y. Orthostatic hypotension: causes, classification, and treatment. Pacing Clin Electrophysiol. 2003 Apr;26(4 Pt 1):892-901. [PubMed: 12715851]
14.
Khurana RK. Coat-hanger ache in orthostatic hypotension. Cephalalgia. 2012 Jul;32(10):731-7. [PubMed: 22711896]
15.
Luukinen H, Koski K, Laippala P, Airaksinen KE. Orthostatic hypotension and the risk of myocardial infarction in the home-dwelling elderly. J. Intern. Med. 2004 Apr;255(4):486-93. [PubMed: 15049883]
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Bookshelf ID: NBK532938PMID: 30422533

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