Orthostatic hypotension

1. Orthostatic hypotension

2. Definition • Committee of the American Autonomic Society and the American Academy of Neurology. • Decline >20 mm Hg in SBP or a decline >10 mm Hg in DBP. • When moves from a supine to a sitting or standing position. • Must be present within 3 minutes after the postural change.

3. Prevalence • 14.8% for those age 65 to 69. • 26% for those age >/= 85. • SBP is > 160 mm Hg, prevalence is higher. • OH occurs in 14.6% of community older. • 52% of nursing home residents.

4. Postural changes in BP • Normal BP response from a supine to a standing position is a small reduction (<10 mm Hg) in SBP and a small increase in DBP (≈2.5 mm Hg). • When stand up from supine , ≈ 500-700 mL of blood is pooled in the lower extremities and in the splanchnic and pulmonary circulations.

5. Postural changes in BP • Decrease in venous return to heart. • Transient reduction in cardiac output. • Stimulation baroreceptors. • Reflexively increases sympathetic tone and vascular resistance. • Inhibits parasympathetic activity resulting in an increased heart rate.

6. Asymptomatic , BP changes without symptoms. • Symptomatic , such as dizziness and faintness occur with BP changes. • Acute or reversible , typically caused by volume loss or medication use. • Chronic or irreversible , caused by endocrine and neurogenic factors.

7. Associated risk factors • DM • HT • Alcoholism • Cardiac diseases • CNS disorders • Dementia • Venous diseases • Amyloidosis

8. Pathogenesis • Impairment of baroreflex. • Thus , excessive reduction in blood volume when upright or inadequate CVS compensation. • Changes in baroreceptor sensitivity, heart rate response , vascular compliance , vasopressin , renin-angiotensin and renal concentrating abilities. • Impaired autonomic reflex arc (afferent, central, or efferent). • Depressed myocardial contractility and vascular responsiveness.

9. Assessment • Fatigue, lightheadedness, falls, and visual blurring when mild reduction in cerebral blood flow. • Syncope, TIA or generalized seizures may occur in more severe cerebral hypoperfusion. • Muscle hypoperfusion can lead to neck pain, LBP and calf claudication. • Cardiac hypoperfusion leads to angina pectoris.

10. Assessment • Medications, alcohol use and review of autonomic, neurologic, cardiovascular and endocrine systems. • Autonomic review, decreased sweating, gastroparesis, incontinence and impotence. • Autonomic failure, symptoms often arise after excessive nocturia or after meal and may worsen during exercise.

13. Assessment • Measure BP & PR after 5 mins of supine rest. • Repeat at 1 and 3 mins. after standing. • Decrease SBP ≥20 mmHg, or DBP ≥10 mmHg with or without an increase in PR is considered an abnormal response. • HR response to postural change can information about the cause of OH. • Minimal change in HR<10 bpm , indicates baroreceptor reflex impairment.

14. Assessment • Tachycardia >20 bpm , indicate volume depletion. • Absence of cardioacceleration does not r/o volume depletion in an older. • Examination of JVP to assess volume status. • Heart auscultation to identify of AS , murmurs and arrhythmias.

15. Assessment • Mental status for dementia, motor examination for stroke and sensory for neuropathies. • Parkinsonism such as bradykinesia, rigidity and tremor. • CBC and stool occult blood test. • BUN and serum creatinine. • Fasting and 2-hour postprandial blood glucose. • ECG. • CT or MRI.

16. Assessment • HR response from supine to standing position and valsalva maneuver. • Cold pressor test. • Plasma norepinephrine levels in response to a postural change. • Tilt-table test is helpful in syncope of unknown cause.

17. Treatment Nonpharmacologic treatments 1.adequate fluid intake, limit or avoid alcohol and exercise regularly in horizontal position. 2. change posture slowly and avoid standing still. 3.spend sitting up each day in prolonged bed rest patients. .

18. Treatment 4.fitted elastic hose or compression stockings. 5.small meals frequently and avoid standing up suddenly. 6.avoid hot showers or excessive heat. 7.avoid straining during micturition and defecation. 8.increase salt intake (without HT).

19. Treatment Pharmacologic treatments 1.Midodrine • Sympathomimetic vasoconstrictor , acts directly on resistance vessels. • Hydrolysis in liver → selective α1–adrenoceptor agonist desglymidodrine. • Significantly increase 1-min standing SBP and improve clinical symptoms of OH.

20. Treatment • Piloerection, paresthesia, urinary retention , pruritus and chills. • 2.5 - 5 mg , effects on BP in supine and standing determined after 1 hour. • Gastroparesis , monitoring after 2 to 3 hr. • Dose titrated according to response. • Starting dose is 2.5 mg at breakfast and lunch or tid ; increased in 2.5 mg steps daily until satisfactory response or dosage of 30-40mg/d.

21. Treatment • Neurogenic hypotension, improvement 47% compared with 28% of placebo. • 10 mg of midodrine increased SBP by a mean of 18 mm Hg. • Contraindicated in severe heart disease such as heartblock, ARF, urinary retention, pheochromocytoma or thyrotoxicosis.

22. Treatment 2.Fludrocortisone • Mineralocorticoid , reduce salt loss and expands plasma volume. • Initial dose 0.1 mg/d , increase at weekly up to 0.4 -1 mg/d. • Edema, hypokalemia and CHF. • Weight gain 2 - 5 pounds and some degree of pedal edema.

23. Treatment • One study (mean age 80) show poor tolerance. • 20% died of unrelated causes. • 33% discontinued after mean of 5 months due to HT, heart failure or depression. • Older patients need to be monitored for signs and symptoms of fluid overload.

24. Treatment 3.Dihydroergotamine • Sympathomimetic vasoconstrictor may increase venous return without increasing arterial pressure. • Long-term use in older should be avoided , potential serious adverse effects associated with ergot alkaloid such as severe vasospasm , gangrene and convulsion.

25. Treatment 4.Erythropoietin • Increases hemoglobin and blood volume. • 1case report show improvement in older. 5.Octreotide • Direct vasoconstriction and increases cardiac output. • DM , pure autonomic failure and multiple system atrophy as well as OH. • Dose 5-50 mcg sc. • Nausea and abdominal cramps. • Expensive and frequent subcutaneous.

26. Treatment 6.Combination therapy • In severe cases, a combination of midodrine and octreotide 7.Pacemaker therapy • OH and bradycardia.

27. Treatment • Diuretics, α-blocker and central α-agonist. • β-adrenergic agonist , ACEI and CCB. • Prevalence of OH with labetalol is 1.4%. • Enalapril(5-20 mg/d) reduces OH episodes, whereas long-acting nifedipine (30-90 mg/d) increases episodes.

28. Treatment Common co-morbidities • Immobility and prolonged bed rest • Falls • Syncope • DM , HT • Parkinson’s Disease • Stroke • Cognitive impairment

29. Treatment Prognosis • Depends on the underlying cause. • Diastolic OH at 1 min and systolic OH at 3 min ,predicts vascular death in older. • OH poor prognosis in DM with HT , risk of death is increased.

30. Treatment Prevention of OH • Diet ●↑intake of Na (5-10 gm/d) and water (not in HT and CHF). ● Eat small, frequent low-carbohydrate (6 small meals instead of 3 large meals) to prevent postprandial worsening of OH. ● ↑ dietary fiber to prevent constipation. ● ↑caffeine intake, as an adenosine receptor blocker ; drink coffee after meals to help prevent the postprandial OH. ● Drink at least 6-8 glasses of water to prevent dehydration; avoid alcohol. ● ↑ intake of salt and fluids during times of heat and febrile illness.

31. Treatment • Physical activity ● Exercise the calf muscles before sitting up, and sit a few min before standing. ● Avoid bending from the floor. ● Wearing waist-length elastic stockings to prevent venous pooling. ● Use a urinal or bedside commode.

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