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W. P. Rivindu H. Wickramanayake
Group no. 04a
6th Year 2nd Semester – 2020 October
Tbilisi State Medical University, Georgia
Orthostasis
● Orthostasis is the presence of at least one of the following: a decrease in
systolic blood pressure by ≥20 mm Hg, a decrease in diastolic blood
pressure by ≥10 mm Hg present within 3 minutes of standing or a head
up tilt table at 60⁰.
● Orthostatic hypotension is a physical sign that warrants diagnosis of its
underlying etiology.
● Common causes of orthostasis are the following:
1) Increasing age.
2) Medications:
- Alpha blockers, diuretics, tricyclics, possibly SSRIs
and atypical antipsychotics.
3) Chronic Autonomic Failure:
- The following figure shows the primary and
secondary causes of chronic autonomic failure.
(Neurogenic orthostatic hypotension)
● Orthostatic hypotension occurs in approximately 20% of patients older than 65 years, increasing
with advancing age.
● The prevalence of symptomatic orthostatic hypotension was found to be 16.2%.
● Orthostasis increases among the elderly in nursing homes to >50%.
● Thirty percent of syncope in the elderly population is because of orthostasis.
● The elderly are susceptible to age-related physiologic changes including the following:
• Decrease in baroreflex sensitivity and overall parasympathetic tone,
• Impairment of alpha adrenergic vasoconstriction,
• Reduction in cardiac and venous compliance,
• Reduction in thirst perception and ability to conserve salt and water, and
• Impaired efficiency of the skeletal muscle pump.
● Orthostasis is associated with an increased risk of cardiovascular disease including stroke,
coronary artery disease, and chronic kidney disease, as well as all-cause mortality among
those aged 55 years and older.
● Because of a more active parasympathetic system, higher estrogen levels, and a lower
center of gravity, women compensate less effectively to orthostasis.
Epidemiology & Risk factors
● Upright posture causes pooling of approximately 500 -700mL of blood in the lower extremities,
pulmonary and splanchnic circulations and interstitial spaces.
● This causes decreased venous return, cardiac output, and arterial pressure, the normal
physiologic response to which is increased carotid baroreceptor activity to increase
sympathetic tone in order to maintain blood pressure.
● Under normal conditions this should not result in a major change in blood pressure.
● This normal reflex is lost in central and peripheral autonomic dysfunction causing
orthostatic hypotension.
● The normal increased heart rate of 10 to 25 beats per minute (bpm) with standing is not seen in
autonomic failure.
● In postural orthostatic tachycardia syndrome (POTS), the heart rate increases by >30 bpm,
with signs of cerebral hypoperfusion.
● In neurocardiogenic syncope, there is increase in vagal activity along with the loss of reflex
efferent sympathetic activity causing bradycardia along with transient orthostasis.
● Decreased sympathetic response to blood pooling in the splanchnic circulation causes
postprandial orthostasis.
Patho-Anatomy & Physiology
● Symptoms may start more subtly with fatigue, impaired cognition,
performance, weakness, leg buckling, and orthostatic dyspnea.
● They can then progress to dizziness, visual disturbance, presyncope, then
syncope/falls.
● Many experience pain in the neck, shoulders or chest.
● It may be aggravated by hot weather of fever, heavy meals, or early
mornings.
● These symptoms are all relieved by recumbence.
● Longitudinal studies show that orthostatic hypotension increases the risk of
stroke, myocardial ischemia, and mortality.
● In the elderly, the higher likelihood of cardiovascular and cerebrovascular
disease and lower renin, angiotensin, and aldosterone levels cause more
severe symptoms; syncope and falls also occur, regardless of symptoms.
Continued;
● Associated with lower cognitive performance in those age >50, especially with supine HTN.
● Uncontrolled HTN as well as orthostatic hypotension worsens fall risk in those over 80.
● In those up to age 80 keeping blood pressure < 140/90 mm/Hg is associated with a decreased
risk for CV morbidity and mortality.
● Syncope-OH is the second most common cause of syncope.
● Reflex syncope (neutrally mediated) is transient loss of consciousness due to a reflex
response that includes vasodilation and/or bradycardia(rarely tachycardia).
● This leads to a systemic hypotension and cerebral hypoperfusion.
● Types - vasovagal, situational, carotid sinus, idiopathic.
● Chronic Orthostatic Intolerance(COI)
- “development of chronic symptoms during upright standing relieved by recumbence,
present on a day-to-day basis. Symptoms must include dizziness or light headedness.”
● POTS-postural orthostatic tachycardia syndrome
- Orthostatic intolerance with excessive increase in heart rate on orthostatic challenge.
- This is a common form of COI that is more common in young women.
- It often affects school and work attendance.
- Both Reflex Syncope and POTS are common with chronic fatigue syndrome
Associated Conditions & Complications
● History
● Physical examination - Blood pressure and heart rate are taken in all 3 positions,
supine, sitting, and standing, with 3- to 5-minute intervals.
● Volume should be assessed by examining mucosa, skin turgor, and jugular venous
pressure.
● The carotid arteries should be examined for bruits.
● Because murmurs in idiopathic hypertrophic cardiomyopathy and mitral valve
prolapse may be more prominent in standing, the heart must be auscultated in
standing too.
● Functional assessment - on loss of function and independence with activities of daily
living (ADLs) and mobility.
● Complete blood count including the following:
● Hemoglobin and hematocrit and folate and cobalamin levels for anemia.
● White blood cell for infection and sepsis and platelet count for bleeding, purpuras,
and ecchymoses.
Evaluation / Diagnosis
● Metabolic panel including the following:
- Electrolytes, blood urea nitrogen, and creatinine to assess volume depletion in
dehydration because of gastroenterological causes, burns, sepsis, and decreased
intake, and overall renal function.
● Investigations may be needed for tabes dorsalis and diabetes in sensory loss, adrenal
insufficiency (morning cortisol levels), and cardiac enzymes (cardiac ischemia)
● Cardiac symptoms including chest pain, dyspnea, and lower extremity edema are worked
up with an electrocardiogram and an echocardiogram.
● Cerebellar symptoms and a suspicion of stroke require work up for ischemic and
hemorrhagic stroke with computerized tomography, magnetic resonance imaging, and
magnetic resonance angiogram.
● Head-up tilt-table testing, which should be ordered when orthostatic hypotension is
suspected in spite of normal blood pressure readings and the patient is unable to stand up
for measurement of orthostatic vital signs.
● The cold pressor test – the normal sympathetic response to immersing the hand in cold
water at 4°C is an increase in systolic blood pressure of 15 mm Hg and diastolic blood
pressure of 10 mm Hg.
Continued;
Rehabilitation Management & Treatments
● The primary goal in treating orthostasis is to decrease the incidence and severity of
postural symptoms rather than achieving upright normotension, because this can lead to
supine hypertension.
● Medical rehabilitation management includes therapeutic approaches subsequently
delineated with an interdisciplinary approach.
● The first therapeutic intervention must be controlling reversible causes and precipitators,
such as high carbohydrate intake, warm weather, alcohol intake, and dehydration.
● Low and colleagues recommend a formal grading scale based on frequency and severity
of symptoms, standing time before onset of symptoms, and influence on ADLs.
● Grade I or II refers to those that might not need drugs, whereas grades III or IV refers to
patients that will need aggressive therapy.
● Grades I-IV are described in the pyramid with accompanying explanation below.
● Pharmacological treatment is necessary in class IV, is recommended in class III, can be
considered in class II, and is generally not recommended in class I patients.
Pharmacotherapeutic interventions :
• Water-500 mL of water intake increases blood pressure by about 40 mm Hg with effects
peaking at 30 minutes, and can last for up to 2 hours.
• Salt added to diet and in the form of tablets. Must monitor fluid and salt intake in patients
with renal disease.
Medication management :
• Fludrocortisone: Synthetic mineralocorticoid. Initial 0.1 mg daily; maximum 1 mg daily.
• Midodrine: Alpha-agonist, selective vasopressor. Initial 2.5 mg on prescription; maximum
10 mg daily. Preferable in patients with supine hypertension and CHF. Should be taken as
needed 30-45 minutes prior to upright activity and it lasts about 2-3 hours. Avoid seated or
supine positioning after dosing and avoid night time dosing.
• Pyridostigmine, a cholinesterase inhibitor, and erythropoietin, which increases red cell
mass and blood volume.
• Droxidopa- affects both symptoms and systolic blood pressure. The long term efficacy is
debatable. Initial dose 100 mg TID at least 3 hours before bedtime. Adverse effects may
include headache, dizziness, nausea and increased hypertension. This was recently approved
by the FDA.
Continued;
Nonpharmacologic interventions:
- Techniques to improve circulation to the brain (used
when there is no balance impairment) include the following:
• Leg crossing prior to standing.
• Dorsiflexion of feet prior to
upright posture.
• Squatting.
• Orthostatic standing training.
Continued;
Support garments:
• Waist high compression stockings and abdominal binders.
• “leg compression alone is not as effective as compression of
the abdomen as the venous component of the lower limbs is
smaller than that of the splanchnic region.”
• Raising the head of the bed by 10 to 20° at night especially
in patients with hypertension.
• Water aerobics and recumbent bicycling help with
reconditioning.
• Tilt table with isometrics.
• Spreading of total carbohydrate intake throughout the day.
Continued;
● A patient-reported orthostatic score is a practical way to monitor
response to treatment.
● Treatment outcomes data, especially pertaining to rehabilitation,
need further research.
● Recently a norepinephrine precursor L-dihydroxy phenylserine
(LDOPS) was shown to be effective in Neurogenic orthostatic
hypotension associated neurodegenerative conditions and is near
FDA approval.
Continued;
● Outcomes depend on the underlying etiology.
● Acute orthostasis is reversible, whereas chronic orthostasis is disabling and difficult to
treat.
● Environmental and behavioral changes help in orthostasis management.
● A urinal or bedside commode so that patients do not have to get up quickly, caffeinated
beverages prior to meals, water intake before standing, and avoiding hot climate improve
symptoms.
● Family and caregivers should be educated to monitor side effects of medication, such as
supine hypertension.
● Other side effects, such as precipitation of congestive heart failure with
mineralocorticoids and urinary obstruction with midodrine, warrant that the support
system involves resources for early detection and management.
● Referrals should be made to a neurologist for autonomic testing when etiology is not
ascertained and to a cardiologist for uncontrolled supine hypertension.
● Consultation should be timely in order to prevent avoidable complications of orthostasis
by facilitating the treatment of reversible causes.
Outcomes
1. https://now.aapmr.org/orthostasis/
2. 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;508-519.
3. Metzler M, Duerr S, Granata R, Krismer F, Robertson D, Wenning G. Neurogenic orthostatic hypotension:
Pathophysiology, evaluation, and management. Journal of Neurology 2012; 2212-2219.
4. Cheng YC. Gender differences in orthostatic hypotension. American Journal of Medical
Science 2011;342:221-225.
5. Arnold AC, Shibao C. Current concepts in orthostatic hypotension management. Current Hypertension
Reports 2013;15.4:304-312.
6. Maule S, Papotti G, Naso D, Magnino C, Testa E, Veglio F. Orthostatic hypotension: evaluation and
treatment. Cardiovascular Hematology Disorders and Drug Targets. 2007 ;7:63-70.
7. Mukai S, Lipsitz LA, Orthostatic hypotension. Clinical Geriatric Medicine.2002;18:253-268.
8. Stewart J. Chronic orthostatic intolerance and the postural tachycardic syndrome(POTS). Journal of
Pediatrics. 2004;145(6)725-730.
9. Low PA. Management of neurogenic orthostatic hypotension: an update. Lancet. 2008;7:451-458.
10. Izcovich A, Gonzalez M, Manzotti M, Catalano HN, Guyatt G. Midodrine for Orthostatic hypotension and
recurrent reflex syncope: A systematic review. Neurology. 2014;83.13:1170-1177.
References
Orthostasis

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Orthostasis

  • 1. W. P. Rivindu H. Wickramanayake Group no. 04a 6th Year 2nd Semester – 2020 October Tbilisi State Medical University, Georgia Orthostasis
  • 2. ● Orthostasis is the presence of at least one of the following: a decrease in systolic blood pressure by ≥20 mm Hg, a decrease in diastolic blood pressure by ≥10 mm Hg present within 3 minutes of standing or a head up tilt table at 60⁰. ● Orthostatic hypotension is a physical sign that warrants diagnosis of its underlying etiology. ● Common causes of orthostasis are the following: 1) Increasing age. 2) Medications: - Alpha blockers, diuretics, tricyclics, possibly SSRIs and atypical antipsychotics. 3) Chronic Autonomic Failure: - The following figure shows the primary and secondary causes of chronic autonomic failure.
  • 4. ● Orthostatic hypotension occurs in approximately 20% of patients older than 65 years, increasing with advancing age. ● The prevalence of symptomatic orthostatic hypotension was found to be 16.2%. ● Orthostasis increases among the elderly in nursing homes to >50%. ● Thirty percent of syncope in the elderly population is because of orthostasis. ● The elderly are susceptible to age-related physiologic changes including the following: • Decrease in baroreflex sensitivity and overall parasympathetic tone, • Impairment of alpha adrenergic vasoconstriction, • Reduction in cardiac and venous compliance, • Reduction in thirst perception and ability to conserve salt and water, and • Impaired efficiency of the skeletal muscle pump. ● Orthostasis is associated with an increased risk of cardiovascular disease including stroke, coronary artery disease, and chronic kidney disease, as well as all-cause mortality among those aged 55 years and older. ● Because of a more active parasympathetic system, higher estrogen levels, and a lower center of gravity, women compensate less effectively to orthostasis. Epidemiology & Risk factors
  • 5. ● Upright posture causes pooling of approximately 500 -700mL of blood in the lower extremities, pulmonary and splanchnic circulations and interstitial spaces. ● This causes decreased venous return, cardiac output, and arterial pressure, the normal physiologic response to which is increased carotid baroreceptor activity to increase sympathetic tone in order to maintain blood pressure. ● Under normal conditions this should not result in a major change in blood pressure. ● This normal reflex is lost in central and peripheral autonomic dysfunction causing orthostatic hypotension. ● The normal increased heart rate of 10 to 25 beats per minute (bpm) with standing is not seen in autonomic failure. ● In postural orthostatic tachycardia syndrome (POTS), the heart rate increases by >30 bpm, with signs of cerebral hypoperfusion. ● In neurocardiogenic syncope, there is increase in vagal activity along with the loss of reflex efferent sympathetic activity causing bradycardia along with transient orthostasis. ● Decreased sympathetic response to blood pooling in the splanchnic circulation causes postprandial orthostasis. Patho-Anatomy & Physiology
  • 6. ● Symptoms may start more subtly with fatigue, impaired cognition, performance, weakness, leg buckling, and orthostatic dyspnea. ● They can then progress to dizziness, visual disturbance, presyncope, then syncope/falls. ● Many experience pain in the neck, shoulders or chest. ● It may be aggravated by hot weather of fever, heavy meals, or early mornings. ● These symptoms are all relieved by recumbence. ● Longitudinal studies show that orthostatic hypotension increases the risk of stroke, myocardial ischemia, and mortality. ● In the elderly, the higher likelihood of cardiovascular and cerebrovascular disease and lower renin, angiotensin, and aldosterone levels cause more severe symptoms; syncope and falls also occur, regardless of symptoms. Continued;
  • 7. ● Associated with lower cognitive performance in those age >50, especially with supine HTN. ● Uncontrolled HTN as well as orthostatic hypotension worsens fall risk in those over 80. ● In those up to age 80 keeping blood pressure < 140/90 mm/Hg is associated with a decreased risk for CV morbidity and mortality. ● Syncope-OH is the second most common cause of syncope. ● Reflex syncope (neutrally mediated) is transient loss of consciousness due to a reflex response that includes vasodilation and/or bradycardia(rarely tachycardia). ● This leads to a systemic hypotension and cerebral hypoperfusion. ● Types - vasovagal, situational, carotid sinus, idiopathic. ● Chronic Orthostatic Intolerance(COI) - “development of chronic symptoms during upright standing relieved by recumbence, present on a day-to-day basis. Symptoms must include dizziness or light headedness.” ● POTS-postural orthostatic tachycardia syndrome - Orthostatic intolerance with excessive increase in heart rate on orthostatic challenge. - This is a common form of COI that is more common in young women. - It often affects school and work attendance. - Both Reflex Syncope and POTS are common with chronic fatigue syndrome Associated Conditions & Complications
  • 8. ● History ● Physical examination - Blood pressure and heart rate are taken in all 3 positions, supine, sitting, and standing, with 3- to 5-minute intervals. ● Volume should be assessed by examining mucosa, skin turgor, and jugular venous pressure. ● The carotid arteries should be examined for bruits. ● Because murmurs in idiopathic hypertrophic cardiomyopathy and mitral valve prolapse may be more prominent in standing, the heart must be auscultated in standing too. ● Functional assessment - on loss of function and independence with activities of daily living (ADLs) and mobility. ● Complete blood count including the following: ● Hemoglobin and hematocrit and folate and cobalamin levels for anemia. ● White blood cell for infection and sepsis and platelet count for bleeding, purpuras, and ecchymoses. Evaluation / Diagnosis
  • 9. ● Metabolic panel including the following: - Electrolytes, blood urea nitrogen, and creatinine to assess volume depletion in dehydration because of gastroenterological causes, burns, sepsis, and decreased intake, and overall renal function. ● Investigations may be needed for tabes dorsalis and diabetes in sensory loss, adrenal insufficiency (morning cortisol levels), and cardiac enzymes (cardiac ischemia) ● Cardiac symptoms including chest pain, dyspnea, and lower extremity edema are worked up with an electrocardiogram and an echocardiogram. ● Cerebellar symptoms and a suspicion of stroke require work up for ischemic and hemorrhagic stroke with computerized tomography, magnetic resonance imaging, and magnetic resonance angiogram. ● Head-up tilt-table testing, which should be ordered when orthostatic hypotension is suspected in spite of normal blood pressure readings and the patient is unable to stand up for measurement of orthostatic vital signs. ● The cold pressor test – the normal sympathetic response to immersing the hand in cold water at 4°C is an increase in systolic blood pressure of 15 mm Hg and diastolic blood pressure of 10 mm Hg. Continued;
  • 10.
  • 11. Rehabilitation Management & Treatments ● The primary goal in treating orthostasis is to decrease the incidence and severity of postural symptoms rather than achieving upright normotension, because this can lead to supine hypertension. ● Medical rehabilitation management includes therapeutic approaches subsequently delineated with an interdisciplinary approach. ● The first therapeutic intervention must be controlling reversible causes and precipitators, such as high carbohydrate intake, warm weather, alcohol intake, and dehydration. ● Low and colleagues recommend a formal grading scale based on frequency and severity of symptoms, standing time before onset of symptoms, and influence on ADLs. ● Grade I or II refers to those that might not need drugs, whereas grades III or IV refers to patients that will need aggressive therapy. ● Grades I-IV are described in the pyramid with accompanying explanation below. ● Pharmacological treatment is necessary in class IV, is recommended in class III, can be considered in class II, and is generally not recommended in class I patients.
  • 12.
  • 13. Pharmacotherapeutic interventions : • Water-500 mL of water intake increases blood pressure by about 40 mm Hg with effects peaking at 30 minutes, and can last for up to 2 hours. • Salt added to diet and in the form of tablets. Must monitor fluid and salt intake in patients with renal disease. Medication management : • Fludrocortisone: Synthetic mineralocorticoid. Initial 0.1 mg daily; maximum 1 mg daily. • Midodrine: Alpha-agonist, selective vasopressor. Initial 2.5 mg on prescription; maximum 10 mg daily. Preferable in patients with supine hypertension and CHF. Should be taken as needed 30-45 minutes prior to upright activity and it lasts about 2-3 hours. Avoid seated or supine positioning after dosing and avoid night time dosing. • Pyridostigmine, a cholinesterase inhibitor, and erythropoietin, which increases red cell mass and blood volume. • Droxidopa- affects both symptoms and systolic blood pressure. The long term efficacy is debatable. Initial dose 100 mg TID at least 3 hours before bedtime. Adverse effects may include headache, dizziness, nausea and increased hypertension. This was recently approved by the FDA. Continued;
  • 14. Nonpharmacologic interventions: - Techniques to improve circulation to the brain (used when there is no balance impairment) include the following: • Leg crossing prior to standing. • Dorsiflexion of feet prior to upright posture. • Squatting. • Orthostatic standing training. Continued;
  • 15.
  • 16. Support garments: • Waist high compression stockings and abdominal binders. • “leg compression alone is not as effective as compression of the abdomen as the venous component of the lower limbs is smaller than that of the splanchnic region.” • Raising the head of the bed by 10 to 20° at night especially in patients with hypertension. • Water aerobics and recumbent bicycling help with reconditioning. • Tilt table with isometrics. • Spreading of total carbohydrate intake throughout the day. Continued;
  • 17. ● A patient-reported orthostatic score is a practical way to monitor response to treatment. ● Treatment outcomes data, especially pertaining to rehabilitation, need further research. ● Recently a norepinephrine precursor L-dihydroxy phenylserine (LDOPS) was shown to be effective in Neurogenic orthostatic hypotension associated neurodegenerative conditions and is near FDA approval. Continued;
  • 18. ● Outcomes depend on the underlying etiology. ● Acute orthostasis is reversible, whereas chronic orthostasis is disabling and difficult to treat. ● Environmental and behavioral changes help in orthostasis management. ● A urinal or bedside commode so that patients do not have to get up quickly, caffeinated beverages prior to meals, water intake before standing, and avoiding hot climate improve symptoms. ● Family and caregivers should be educated to monitor side effects of medication, such as supine hypertension. ● Other side effects, such as precipitation of congestive heart failure with mineralocorticoids and urinary obstruction with midodrine, warrant that the support system involves resources for early detection and management. ● Referrals should be made to a neurologist for autonomic testing when etiology is not ascertained and to a cardiologist for uncontrolled supine hypertension. ● Consultation should be timely in order to prevent avoidable complications of orthostasis by facilitating the treatment of reversible causes. Outcomes
  • 19. 1. https://now.aapmr.org/orthostasis/ 2. 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;508-519. 3. Metzler M, Duerr S, Granata R, Krismer F, Robertson D, Wenning G. Neurogenic orthostatic hypotension: Pathophysiology, evaluation, and management. Journal of Neurology 2012; 2212-2219. 4. Cheng YC. Gender differences in orthostatic hypotension. American Journal of Medical Science 2011;342:221-225. 5. Arnold AC, Shibao C. Current concepts in orthostatic hypotension management. Current Hypertension Reports 2013;15.4:304-312. 6. Maule S, Papotti G, Naso D, Magnino C, Testa E, Veglio F. Orthostatic hypotension: evaluation and treatment. Cardiovascular Hematology Disorders and Drug Targets. 2007 ;7:63-70. 7. Mukai S, Lipsitz LA, Orthostatic hypotension. Clinical Geriatric Medicine.2002;18:253-268. 8. Stewart J. Chronic orthostatic intolerance and the postural tachycardic syndrome(POTS). Journal of Pediatrics. 2004;145(6)725-730. 9. Low PA. Management of neurogenic orthostatic hypotension: an update. Lancet. 2008;7:451-458. 10. Izcovich A, Gonzalez M, Manzotti M, Catalano HN, Guyatt G. Midodrine for Orthostatic hypotension and recurrent reflex syncope: A systematic review. Neurology. 2014;83.13:1170-1177. References