Orthostatic hypotension: causes, diagnosis and treatment | Clinique Omicron<\/title>\n<meta name=\"description\" content=\"Orthostatic hypotension is a drop in blood pressure on rising. Causes, etiological assessment, non-pharmacological measures, fludrocortisone, midodrine and management in Quebec.\">\n<meta name=\"keywords\" content=\"hypotension orthostatique traitement, hypotension posturale, chute pression art\u00e9rielle lever, fludrocortisone midodrine, syncope orthostatique, dysautonomie, hypotension orthostatique \u00e2g\u00e9, hypotension orthostatique Qu\u00e9bec\">\n<link rel=\"preconnect\" href=\"https:\/\/fonts.googleapis.com\">\n<link href=\"https:\/\/fonts.googleapis.com\/css2?family=Cinzel:wght@600&family=Poppins:wght@400;500;600;700&display=swap\" rel=\"stylesheet\">\n<style>\n.co-wrap * { font-family: 'Poppins', sans-serif; box-sizing: border-box; }\n.co-wrap { max-width: 1100px; margin: 0 auto; padding: 30px 0 60px; }\n.co-label { font-family: 'Cinzel', serif; font-size: 14px; font-weight: bold; letter-spacing: 1px; text-transform: uppercase; color: #4D6577; margin-bottom: 14px; display: block; }\n.co-wrap h1 { font-size: 32px; font-weight: 500; color: #323C52; margin: 0 0 22px; line-height: 1.2; }\n.co-intro { font-size: 16px; line-height: 1.75; color: #4D6577; margin-bottom: 36px; padding-bottom: 32px; border-bottom: 1px solid rgba(77,101,119,.2); }\n.co-wrap h2 { font-size: 20px; font-weight: 600; color: #323C52; margin: 32px 0 12px; }\n.co-wrap p { font-size: 15px; color: #4D6577; line-height: 1.7; margin-bottom: 14px; }\n.co-list { list-style: none; padding: 0; margin: 12px 0 24px; }\n.co-list li { font-size: 15px; color: #4D6577; padding: 10px 14px 10px 38px; margin-bottom: 8px; border-radius: 6px; position: relative; background: rgba(77,101,119,.06); border-left: 3px solid #4D6577; }\n.co-list li::before { content: \"\u2713\"; position: absolute; left: 12px; font-weight: 700; color: #4D6577; }\n.co-table { width: 100%; border-collapse: collapse; margin: 14px 0 22px; font-size: 14px; border-radius: 8px; overflow: hidden; table-layout: fixed; }\n.co-table thead tr { background: #323C52; color: #fff; }\n.co-table thead th { padding: 11px 16px; text-align: left; font-weight: 600; font-size: 13px; }\n.co-table tbody tr:nth-child(even) { background: rgba(77,101,119,.06); }\n.co-table tbody tr:nth-child(odd) { background: #fff; }\n.co-table td { padding: 10px 16px; color: #4D6577; border-bottom: 1px solid rgba(77,101,119,.12); font-size: 14px; vertical-align: top; }\n.co-table td:first-child { font-weight: 600; color: #323C52; }\n.co-infobox { display: flex; gap: 12px; background: rgba(77,101,119,.06); border-radius: 8px; border-left: 4px solid #4D6577; padding: 14px 18px; margin: 18px 0 28px; font-size: 14px; color: #4D6577; line-height: 1.65; }\n.co-infobox .ico { font-size: 18px; flex-shrink: 0; }\n.co-urgence { background: #fff8f8; border-left: 5px solid #c0392b; border-radius: 6px; padding: 20px 26px; margin: 24px 0 32px; }\n.co-urgence .co-urgence-titre { font-size: 13px; font-weight: 700; color: #c0392b; letter-spacing: 1.5px; text-transform: uppercase; margin-bottom: 10px; }\n.co-urgence p { color: #5a2020; font-size: 14px; margin: 0 0 10px; line-height: 1.7; }\n.co-urgence p:last-child { margin-bottom: 0; }\n.co-disclaimer { font-size: 13px; color: #8a9aaa; font-style: italic; border-top: 1px solid rgba(77,101,119,.15); padding-top: 24px; margin-top: 40px; line-height: 1.6; }\n<\/style>\n<\/head>\n<body>\n<div class=\"co-wrap\">\n <span class=\"co-label\">Neurology & Internal Medicine & Family Medicine & Geriatrics<\/span>\n <h1>Orthostatic hypotension<\/h1>\n\n <div class=\"co-intro\">\n Orthostatic hypotension (OH) is defined as a fall in systolic blood pressure (SBP) of at least 20 mmHg or diastolic blood pressure (DBP) of at least 10 mmHg within 3 minutes of going from lying to standing, with or without symptoms. This consensus definition, established by the European Society of Cardiology and the American Autonomic Society (Freeman 2011 - Journal of the American College of Cardiology), is based on standardized sphygmomanometric measurement. HO results from a maladaptation of the autonomic nervous system and vascular regulatory mechanisms to the gravitational redistribution of blood on rising: normally, the transition to orthostatism results in a venous pooling of 500 to 700 mL in the lower limbs and splanchnic territory, a reduction in venous return and systolic ejection volume, compensated within seconds by sympathetic baroreflex activation (tachycardia + arterial and venous vasoconstriction) and release of noradrenaline, renin and vasopressin. HO occurs when this compensation is insufficient. Its prevalence increases sharply with age - from 5 % before 50 to 30 % after 70 - and represents one of the major causes of falls, syncope, fractures and loss of autonomy in the elderly. HO is also an independent prognostic marker of cardiovascular mortality and cerebrovascular events (Eigenbrodt 2000 - Stroke). In addition to the classic immediate form, there are initial forms (fall within the first minute, often unrecognized because not routinely measured) and delayed forms (after 3-10 minutes), as well as Postural Orthostatic Tachycardia Syndrome (POTS), a distinct entity preferentially affecting young women.\n <\/div>\n\n <h2>Pathophysiology, etiologies and clinical presentation<\/h2>\n <ul class=\"co-list\">\n <li><strong>Mechanisms of normal orthostatic blood pressure regulation and pathophysiology of HO :<\/strong> normal response on rising (chronology): 0-30 seconds: venous pooling \u2192 reduction in venous return \u2192 drop in ejection volume (-40 %) \u2192 transient fall in BP \u2192 immediate activation of carotid and aortic baroreceptors \u2192 reflex sympathetic discharge \u2192 tachycardia (HR +10-25 bpm) + arteriolar and venous vasoconstriction \u2192 30 seconds - 2 minutes: noradrenalin secretion + RAAS activation (renin \u2192 angiotensin II \u2192 aldosterone) + vasopressin (ADH) \u2192 consolidation of vasoconstriction + 2-10 minutes: complete normalization of BP \u2192 prolonged standing \u2192 active calf muscle mechanisms (venous muscle pump); pathophysiology of HO: baroreceptor reflex arc defect (most common): damage to efferent sympathetic fibers (autonomic neuropathy) \u2192 no adequate vasoconstriction \u2192 uncompensated fall in BP \u2192 in diabetic neuropathy + amyloidosis + multisystem atrophy (MSA) + Parkinson's disease \u2192 absolute hypovolemia: reduction in circulating blood volume \u2192 insufficient supply to the baroreflex \u2192 dehydration + adrenal insufficiency + hemorrhage + drug causes: drugs are the leading cause of acquired HO in clinical practice \u2192 alpha-adrenergic blockade (alpha-blockers + antipsychotics) \u2192 baroreflex blockade (beta-blockers) \u2192 volume reduction (diuretics) \u2192 direct vasodilation (nitrate derivatives + ACE inhibitors + calcium antagonists) \u2192 other mechanisms; specific features of HO in the elderly: less sensitive baroreflex (less compliant arteries) + reduced renal response to aldosterone + decreased thirst \u2192 tendency to chronic hypovolemia + polypharmacy + multiple comorbidities \u2192 HO in 30 % of institutionalized elderly (Rutan 1992 - Hypertension) \u2192 association HO + risk of falling \u00d7 2.6 (Gangavati 2011 - Archives of Internal Medicine) \u2192 mortality: Eigenbrodt 2000 - Stroke: HO \u2192 risk of stroke \u00d7 2.0 + risk of death \u00d7 1.36 over 10 years \u2192 postprandial orthostatic hypotension: worsening of HO in the 60-90 min following a meal \u2192 uncompensated postprandial mesenteric vasodilation \u2192 frequent in the elderly + Parkinson + dysautonomia \u2192 light + small + fractionated meals \u2192 avoid alcohol with meals<\/li>\n <li><strong>Etiological classification - neurogenic, drug-induced and systemic causes :<\/strong> Neurogenic HO (dysautonomia) - most severe and hardest to treat: primary dysautonomias - degenerative: multisystem atrophy (MSA): synucleinopathy \u2192 degeneration of preganglionic sympathetic neurons of the vasomotor center \u2192 severe HO + Parkinson's (OH in 20-50 %) + dementia with Lewy bodies (DCL) + pure Parkinson's disease \u2192 secondary dysautonomias (autonomic neuropathies): diabetes (diabetic autonomic neuropathy - 25-30 % of type 1 diabetics + 15-20 % of type 2) \u2192 most frequent form of secondary dysautonomia \u2192 amyloidosis (AL + transthyretin) \u2192 accumulation of amyloid fibrils in autonomic nerves + vessels \u2192 severe HO \u2192 HIV \u2192 paraneoplastic syndromes (anti-HU + anti-VGCC + anti-ganglial - autoimmune autonomic ganglionopathy) \u2192 chronic alcoholism \u2192 rare infiltrative diseases (sarcoidosis + leprosy) ; drug-induced causes (leading cause of acquired HO in practice): diuretics (thiazides + furosemide) \u2192 hypovolemia \u2192 alpha-blockers (tamsulosin + doxazosin + alfuzosin) \u2192 arteriolar vasodilation \u2192 HO ++ \u2192 central antihypertensives (clonidine + methyldopa) \u2192 central sympathetic inhibition \u2192 antipsychotics (risperidone + haloperidol + chlorpromazine + olanzapine) \u2192 alpha blockade1 + anticholinergic \u2192 HO ++ \u2192 tricyclic antidepressants (imipramine + amitriptyline) \u2192 alpha-blockade1 + anticholinergic \u2192 MAOI \u2192 noradrenaline depletion + nitrate derivatives (nitroglycerin + isosorbide) \u2192 massive venous vasodilation \u2192 calcium-channel blockers (amlodipine + nifedipine) + ACEI\/ARA-2 \u2192 vasodilation \u2192 worsening of HO \u2192 levodopa + dopaminergic agonists (pramipexole + ropinirole) in Parkinson \u2192 vasodilation + sympathetic inhibition \u2192 opioids \u2192 sympathetic inhibition + vasodilation \u2192 anesthetics (spinal anesthesia + epidural + general agents) ; non-drug systemic causes: dehydration (very frequent causes): gastroenteritis + diaphoresis + insufficient intake \u2192 adrenal insufficiency (adrenal crisis): low cortisol \u2192 insufficient RAAS + reduced vascular response \u2192 severe HO + hyponatremia + abdominal pain \u2192 emergency \u2192 acute hemorrhage \u2192 absolute hypovolemia \u2192 cardiac insufficiency (reduced output) \u2192 venous causes: major varicose veins + prolonged bed rest (deconditioning + reduced plasma volume) + pregnancy (vasodilation + compression cave) + POTS (postural orthostatic tachycardia syndrome) : entity distinct from HO \u2192 tachycardia \u226530 bpm on rising (or HR \u2265120 bpm) without significant BP drop \u2192 young women (15-50 years) \u2192 pathophysiology: relative hypovolemia + distal autonomic neuropathy + compensatory sympathetic hyperactivity \u2192 post-COVID: marked increase in POTS cases since 2020 (Taub 2022 - Nature Reviews Cardiology)<\/li>\n <li><strong>Clinical presentation, standardized measurements and additional tests :<\/strong> HO symptoms : classically within the first 3 minutes of rising \u2192 lipothymia (sensation of impending malaise + blurred vision + vertigo) + pre-syncope (dizziness + instability) + syncope (brief loss of consciousness) + tunnel vision + tinnitus + occipital headache (\u00abcoat hanger headache\u00bb - pain in a hanger over the neck and shoulders \u2192 insufficient irrigation of the paravertebral muscles by the vertebral artery) + generalized weakness + falling + nausea \u2192 asymptomatic HO: documented BP drop without symptoms \u2192 frequent \u2192 prognosis less favorable than no HO but fewer immediate falls; standardized measurement of orthostatic BP (ESC 2018 + Freeman 2011 JACC): strict supine \u22655 minutes \u2192 measure BP supine \u2192 stand up active \u2192 measure BP at 1 min + 3 min orthostatically (and at 5 min if available) \u2192 take HR into account at each measurement \u2192 HO confirmed if: PAS fall \u226520 mmHg or PAD \u226510 mmHg within 3 min \u2192 initial (early) HO: fall \u226540 mmHg within the first 15-30 seconds \u2192 not documented by measurement at 1 min \u2192 requires continuous BP monitoring (Finapres + Task Force Monitor) \u2192 delayed (delayed) HO: fall \u226520\/10 mmHg appearing after 3 minutes of rising \u2192 documented by measurement at 5-10 min \u2192 often in elderly subjects with mild neurogenic HO \u2192 tilt test (tilt table): measurement of BP and HR in supine position + tilt at 60-70\u00b0 for 20-45 min \u2192 documented continuous BP + HR \u2192 diagnosis of hard-to-detect forms of HO + vasovagal syncope (syncope within the first 20 minutes on tilt-test) + POTS (tachycardia \u226530 bpm without syncope); targeted etiological workup according to clinic: CBC (anemia) + ionogram + creatinine (eGFR) + glycemia + HbA1c (diabetes) + morning cortisol (adrenal insufficiency) + TSH (hypothyroidism + hyperthyroidism) + renal workup + proteinuria (amyloidosis) + plasma catecholamine assay, supine and standing + plasma norepinephrine assay, supine and standing (in specialized center): noradrenaline not rising on rising \u2192 peripheral dysautonomia (AMS type P or Parkinson) vs excessive rise \u2192 compensatory sympathetic hyperactivity \u2192 ECG + Holter: arrhythmias causing syncope \u2192 24h ambulatory pressure Holter (ABPM): assessment of nocturnal blood pressure profile (nocturnal hypertension often associated with HO in dysautonomias) \u2192 sweating test + Valsalva reflex (in autonomic laboratory) + cerebral MRI if associated neurological signs <\/ul>\n\n <h2>Management - non-pharmacological measures and treatments<\/h2>\n <table class=\"co-table\">\n <colgroup><col style=\"width:200px;\"><col style=\"width:42%;\"><col><\/colgroup>\n <thead>\n <tr><th>Treatment \/ intervention<\/th><th>Mechanism and practical details<\/th><th>Evidence and follow-up<\/th><\/tr>\n <\/thead>\n <tbody>\n <tr>\n <td>Non-pharmacological measures - Universal 1st line<br><small style=\"font-weight:400;color:#7a8fa0;\">Hydration - salt - counter-pressure - gradual rising - split meals - compression stockings<\/small><\/td>\n <td>Behavioral measures and patient education - ESC 2018 + AAN (American Academy of Neurology) 2017 recommendations: sufficient hydration: target 2-2.5 L\/d of fluids \u2192 water, broths, juices \u2192 rapid correction of hypovolemic HO \u2192 hydration bolus of 500 mL of cold water ingested rapidly (over 2-5 min) \u2192 increase in systolic BP of 20-35 mmHg over 20-30 min \u2192 mechanism: orthostatic reflex via osmostimulation of the gastrointestinal tract \u2192 useful in anticipated HO situations (meals + early rising) \u2192 Jordan 2000 - Circulation: demonstration of the pressor reflex of ingested water + increased sodium intake: dietary salt 6-10 g\/d (vs. 5-6 g recommended in HTA) \u2192 increases blood volume \u2192 BUT contraindicated if IC + severe HTA + advanced CKD \u2192 NaCl tablets 1 g \u00d7 3\/d alternatively if insufficient nutrition; physical counterpressure maneuvers (PCM): leg crossing + isometric contraction of leg and gluteal muscles + squat (squatting briefly) + pumping feet alternately \u2192 mechanism: compression of lower limb veins \u2192 reduction in venous pooling \u2192 increase in venous return \u2192 increase in BP by 10-30 mmHg \u2192 van Lieshout 2000 - Journal of Applied Physiology: PCM \u2192 increase in systolic BP +20 mmHg \u2192 Brignole 2004 - Journal of the American College of Cardiology: PCM \u2192 reduction in vasovagal syncope in the PC-Trial; progressive rising and behavioral education: get up in 3 stages (sitting position at the edge of the bed \u2192 wait 30-60 seconds with feet on the floor \u2192 get up) + avoid rapid nocturnal getting up (greatest vulnerability is in the morning when getting up after a night) + avoid hot environments (heat \u2192 cutaneous vasodilation \u2192 worsens HO) + avoid alcohol (vasodilation + inhibition of the baroreflex) + avoid intense exertion on an empty stomach + compression stockings and compressive clothing: class II-III compression stockings (30-40 mmHg) up to the thigh \u2192 reduce venous pooling in the lower limbs \u2192 effective if worn early in the morning (before getting up if possible) \u2192 modest effectiveness in practice (often poor tolerance in the elderly) + abdominal binder: compression of splanchnic territory \u2192 complementary mechanism \u2192 can be combined with compression stockings \u2192 more tolerated than stockings \u2192 Smit 2004 - Journal of Neurology Neurosurgery and Psychiatry: stockings + belt \u2192 12 mmHg BP improvement + elevation of head of bed (30\u00b0): counterintuitive but effective in severe dysautonomia \u2192 reduces nocturnal diuresis + improves plasma volume \u2192 must be associated with raised head of bed (no tilting of whole mattress) \u2192 fractionated and small meals: postprandial HO \u2192 5-6 small meals\/d vs 3 large \u2192 reduced carbohydrate load per meal \u2192 coffee or caffeine before meals: vasoconstriction + pressor effect \u2192 200-250 mg (1-2 cups) before main meal \u2192 effective in postprandial HO<\/td>\n <td>Medication review - key step often undervalued: systematically review ALL the patient's medications before initiating pharmacological treatment of HO \u2192 medications to be reduced or stopped as a priority: diuretics (furosemide + hydrochlorothiazide + indapamide) \u2192 reduce or stop if symptomatic HO \u2192 particularly in the elderly patient + alpha-blockers (tamsulosin + alfuzosin + doxazosin) \u2192 BPH \u2192 alternatives: 5-ARI inhibitors (finasteride) + centrally acting dual antihypertensives (clonidine + methyldopa) \u2192 less hypotensive alternatives + tricyclic antidepressants \u2192 alternatives: SSRIs (less hypotensive) + beta-blockers + calcium channel blockers \u2192 reassess indication and dose + nitrates \u2192 use only on demand if possible + opioid analgesics \u2192 reduce if possible + assess benefit-risk balance; 24h ABPM to detect associated nocturnal hypertension: patients with severe dysautonomia (AMS + Parkinson + diabetic neuropathy) often present paradoxical nocturnal hypertension (reverse dipping) \u2192 elevated nocturnal BP \u2192 risk of nocturnal stroke \u2192 nocturnal diuretics sometimes indicated despite diurnal HO \u2192 complex management \u2192 autonomic specialist \u2192 elevation of head of bed \u2192 reduces nocturnal pressure + improves diurnal HO (renal aldosterone mechanism); exercise and reconditioning: pool exercise (aquatherapy): horizontal positioning + hydrostatic pressure \u2192 maintains plasma volume \u2192 avoids orthostatic drop during exercise + recumbent or supine bike exercise \u2192 avoid standing until sufficient conditioning + progressive orthostatic training (tilt training) \u2192 improves baroreflex sensitivity + venous deconditioning \u2192 useful in POTS + lower limb strengthening exercise \u2192 improves venous muscle pumping<\/td>\n <\/tr>\n <tr>\n <td>Fludrocortisone - mineralocorticoid<br><small style=\"font-weight:400;color:#7a8fa0;\">Volume expansion - 0.1-0.3 mg\/d - hypokalemia - edema - nocturnal hypertension<\/small><\/td>\n <td>Fludrocortisone mechanism of action: synthetic aldosterone analog \u2192 strong mineralocorticoid effect (300\u00d7 endogenous aldosterone) \u2192 weak glucocorticoid effect \u2192 binding to mineralocorticoid receptor in collecting tubule \u2192 Na\u207a reabsorption + K\u207a excretion \u2192 plasma volume expansion \u2192 increased venous return \u2192 improved orthostatic BP \u2192 beneficial accessory effects: sensitization of vascular alpha-adrenergic receptors to noradrenaline \u2192 improvement of reflex vasoconstriction \u2192 dosage: 0.05-0.3 mg\/d po \u2192 start at 0.05-0.1 mg\/d \u2192 gradual increase every 1-2 weeks depending on response and tolerance \u2192 maximum effect expected at 1-2 weeks \u2192 usual maximum dose: 0.3-0.4 mg\/d (beyond that \u2192 significant side effects with no additional benefit) \u2192 taken in the morning (to minimize nocturnal hypertension); preferred indications: neurogenic dysautonomia (AMS + autonomic neuropathy + Parkinson + relative adrenal insufficiency) \u2192 relative hypovolemic HO (POTS + deconditioning) \u2192 efficacy in clinical trials: Logan 1966 - Circulation: first trials showing efficacy in dysautonomia + meta-analyses and systematic reviews (Figueroa 2010 - Clinical Autonomic Research): fludrocortisone \u2192 improvement in orthostatic BP + reduction in symptoms + moderate level of evidence (few large randomized trials) \u2192 CHSA Trial (Lahrmann 2006 - Movement Disorders): fludrocortisone + domperidone in AMS \u2192 modest improvement \u2192 main side effects: hypokalemia (monitor kalemia + K\u207a supplementation if <3.5 mmol\/L) + fluid retention \u2192 peripheral edema + decubitus hypertension (nocturnal hypertension) \u2192 special attention in patients with mild IC \u2192 worsening of heart failure \u2192 relative contraindications: decompensated heart failure + severe CKD (eGFR <30) + severe uncontrolled hypertension + pre-existing hypokalemia \u2192 biological monitoring: kalemia + creatinine + supine and standing BP \u2192 at 2 weeks + 1 month + 3 months + then quarterly<\/td>\n <td>Comparative efficacy and place in therapeutic strategy: fludrocortisone is often considered the 1st-line agent in severe dysautonomias despite a moderate level of evidence \u2192 its benefit is best documented in adrenal insufficiency (formal indication) + in primary neurogenic dysautonomias \u2192 in drug-induced or hypovolemic HO \u2192 etiological treatment as a priority \u2192 fludrocortisone as temporary support if necessary \u2192 in POTS \u2192 fludrocortisone effective in increasing blood volume \u2192 but may worsen reflex tachycardia \u2192 combine with low-dose beta-blockers (propranolol 10-20 mg) in POTS \u2192 CHAMP trial (Taub 2021 - NEJM : pediatric randomized trial) \u2192 in pediatric POTS: propranolol + fludrocortisone \u2192 both superior to placebo on symptoms + ivabradine as an alternative if beta blockers poorly tolerated in POTS \u2192 frequently used combinations: fludrocortisone + midodrine (synergistic benefit on standing BP) + fludrocortisone + pyridostigmine + droxidopa in AMS \u2192 polypharmacy necessary in severe forms<\/td>\n <\/tr>\n <tr>\n <td>Midodrine - alpha-1 adrenergic agonist<br><small style=\"font-weight:400;color:#7a8fa0;\">Vasoconstriction - 2.5-10 mg \u00d7 3\/d - decubitus hypertension - urinary retention - piloerection<\/small><\/td>\n <td>Mechanism and pharmacological profile of midodrine: direct alpha-1 adrenergic receptor agonist \u2192 peripheral arteriolar and venous vasoconstriction \u2192 increased peripheral vascular resistance \u2192 increased BP \u2192 prodrug: metabolized to desglymidodrine (active metabolite) \u2192 half-life: 2-3h \u2192 maximum effect 1h after intake \u2192 duration of action: 3-4h \u2192 does not cross the blood-brain barrier (advantage: no central effects) \u2192 no direct cardiac action (no tachycardia); dosage and administration: start at 2.5 mg \u00d7 2\/d \u2192 increase to 2.5-10 mg \u00d7 3\/d according to response and tolerance \u2192 intakes: morning + midday + late afternoon \u2192 NEVER take late evening or at bedtime (risk of severe nocturnal decubitus hypertension) \u2192 avoid in the 4h preceding bedtime \u2192 take 15-30 min before risk situations (getting up + eating) \u2192 FDA 1996 approval (Mathias 1995 - Lancet : randomized trial \u2192 midodrine \u00d7 4 weeks \u2192 improvement in orthostatic BP and symptoms) \u2192 Health Canada approval \u2192 RAMQ reimbursement (exception drug or regular list depending on formulation) \u2192 clinical efficacy: Jankovic 1993 - Neurology + Wright 1998 - JAMA Internal Medicine: midodrine \u2192 improvement in orthostatic BP +22 mmHg (systolic) vs placebo \u2192 improvement in symptoms (lipothymia + dizziness + syncope) \u2192 non-inferiority trial vs fludrocortisone \u2192 comparable with different safety profile; contraindications to midodrine: severe hypertension (systolic BP >180 mmHg at rest) + heart failure \u2192 worsening preload + significant urinary retention (urethral alpha-1 agonist \u2192 urethral sphincter contraction) + pheochromocytoma + hyperthyroidism + severe coronary disease + severe renal insufficiency (accumulation)<\/td>\n <td>Midodrine side effects and clinical management: decubitus hypertension (supine hypertension): pressor effect persists in supine position \u2192 significant + sometimes severe hypertension \u2192 main limiting side effect \u2192 absolute rule: never take before bedtime + always measure supine BP before each prescription \u2192 if nocturnal hypertension \u2192 reduce afternoon dose + elevate head of bed + piloerection (goose bumps) + scalp itching : alpha-1 effect on hair erector muscles \u2192 frequent + benign \u2192 may alert patient to drug efficacy + urinary retention: urethral alpha-1 effects + caution if BPH + check RPM if urinary symptoms + paresthesias + cold sensation of extremities (excessive vasoconstriction) \u2192 reduce dose + mild reflex bradycardia: vasoconstriction \u2192 slight increase in resistances \u2192 reflex decrease in HR \u2192 rare but watch for BAV; therapeutic associations and combinations in severe HO: midodrine + fludrocortisone \u2192 most frequent combination in SMA and severe dysautonomias \u2192 synergistic benefit (increased blood volume + vasoconstriction) \u2192 midodrine + pyridostigmine \u2192 pyridostigmine (acetylcholinesterase inhibitor) \u2192 increases sympathetic tone via the autonomic nervous system \u2192 Sandroni 2006 - Clinical Pharmacology and Therapeutics : pyridostigmine 30-60 mg \u00d7 3\/d \u2192 improvement of neurogenic HO without worsening nocturnal HTA (major advantage vs fludrocortisone) \u2192 midodrine + droxidopa (in AMS and Parkinson's disease) \u2192 triple combination in the most severe forms<\/td>\n <\/tr>\n <tr>\n <td>Droxidopa and other agents - AMS, Parkinson, POTS<br><small style=\"font-weight:400;color:#7a8fa0;\">Droxidopa - pyridostigmine - octreotide - erythropoietin - beta-blockers POTS<\/small><\/td>\n <td>Droxidopa (Northera) - noradrenaline precursor: mechanism: oral noradrenaline precursor \u2192 converted by DOPA decarboxylase into noradrenaline \u2192 acts directly on peripheral and central adrenergic receptors \u2192 restores noradrenaline levels in sympathetic synapses \u2192 specifically indicated in dysautonomias with noradrenaline depletion : dopamine beta-hydroxylase deficiency (DBH - very rare) + AMS + pure autonomic failure (PAF) + Parkinson's with refractory HO \u2192 FDA 2014 approval (ADAPT study - Kaufmann 2014 - New England Journal of Medicine : droxidopa \u2192 improvement of HO symptoms and orthostatic BP in neurogenic HO) \u2192 not available in RAMQ drug list at time of data - check current availability \u2192 dosage: 100 mg \u00d7 3\/d \u2192 titration up to 600 mg \u00d7 3\/d \u2192 side effects: decubitus hypertension + headache + nausea + fatigue; pyridostigmine (Mestinon): acetylcholinesterase inhibitor \u2192 increases acetylcholine in autonomic synapses \u2192 potentiates reflex sympathetic tone via autonomic ganglia \u2192 unique advantage: improves standing HO WITHOUT significantly worsening supine BP \u2192 unlike midodrine and fludrocortisone \u2192 Singer 2006 - Annals of Internal Medicine: pyridostigmine 30-60 mg \u00d7 3\/d \u2192 improves standing BP without nocturnal hypertension \u2192 indication: neurogenic HO with associated nocturnal hypertension (situation where midodrine and fludrocortisone are difficult to use) + side effects: diarrhea + abdominal cramps + hypersalivation + bronchospasm (caution if asthma\/BPCO) + fasciculations \u2192 dosage: 30 mg \u00d7 3\/d \u2192 up to 60 mg \u00d7 3\/d; octreotide (long-acting somatostatin): inhibits postprandial mesenteric vasodilation + inhibits release of intestinal vasodilatory peptides \u2192 indicated specifically in refractory postprandial HO \u2192 25-50 \u00b5g SC before meals \u2192 disadvantage: subcutaneous route + digestive effects (nausea + biliary lithiasis); recombinant erythropoietin (EPO): stimulates erythropoiesis \u2192 increases total blood volume \u2192 useful in HO associated with anemia + in AMS and pure autonomic failure with mild anemia \u2192 little robust data + high cost; POTS - specific treatment: low-dose beta-blockers (propranolol 10-20 mg) \u2192 reduce reflex tachycardia without further lowering BP + ivabradine (5 mg \u00d7 2\/d - off MA): If inhibitor \u2192 reduces tachycardia without vascular effect \u2192 Barzilai 2019 - European Heart Journal Case Reports + treatment of cause: post-COVID autonomic neuropathy \u2192 fludrocortisone + reconditioning + compression<\/td>\n <td>Management of nocturnal hypertension in patients with diurnal HO - therapeutic paradox: frequent problem in severe dysautonomias: severe diurnal HO + nocturnal HTA (reverse dipping) \u2192 risk of nocturnal stroke \u2192 difficult to treat simultaneously \u2192 strategies: elevation of head of bed to 30\u00b0 \u2192 reduces nocturnal HTA (renal redistribution of blood + reduced filtration pressure) \u2192 improves diurnal HO (maintenance of plasma volume) \u2192 most effective measure for both components + nocturnal nitroglycerin patch (0.1-0,2 mg\/h) \u2192 if severe nocturnal HTA \u2192 to be removed in the morning \u2192 mineralocorticoid receptor antagonist (losartan) in the evening \u2192 reduction of nocturnal HTA without worsening morning HO \u2192 Omboni 2006 - Hypertension + pyridostigmine (does not cause nocturnal HTA) \u2192 advantage over midodrine + fludrocortisone \u2192 change timing of midodrine doses (avoid late afternoon dose) ; long-term monitoring and follow-up of HO: 24h ABPM: every 6-12 months \u2192 nocturnal profile assessment + falls score (Morse + Tinetti) + autonomy assessment \u2192 symptom diary (frequency of lipothymia + syncope + falls) \u2192 neurological reassessment if progressive HO (AMS + Parkinson's) \u2192 adaptation of technical aids (cane + walker + lift chair) \u2192 caregiver education + home occupational therapy (securing the environment + mats + grab bars)<\/td>\n <\/tr>\n <\/tbody>\n <\/table>\n\n <div class=\"co-infobox\">\n <span class=\"ico\">\u2139\ufe0f<\/span>\n <span><strong>Medication revision is the first step in treating orthostatic hypotension:<\/strong> drugs - diuretics, alpha-blockers, central antihypertensives, antipsychotics, tricyclic antidepressants, nitrates, opioids - represent the leading cause of acquired HO in clinical practice. Before adding pharmacological treatment to HO, it is essential to identify and reduce or stop non-essential hypotensive drugs, particularly in elderly patients on polymedication. Even a modest reduction in dose can eliminate HO without the need to add a new drug.<\/span>\n <\/div>\n\n <div class=\"co-urgence\">\n <div class=\"co-urgence-titre\">Situations requiring urgent medical assessment<\/div>\n <p><strong>Syncope on rising + head trauma + high-kinetic fall (suspected hip fracture) + prolonged loss of consciousness (>1-2 minutes) + persistent post-syncope confusion<\/strong> \u2192 call 911 + emergency room assessment \u2192 cranial CT scan if trauma + hip X-ray + etiological assessment of syncope \u2192 ECG + cardiac monitoring \u2192 do not leave patient alone until medical assessment.<\/p>\n <p><strong>HO severe + hyponatremia + hyperkalemia + tanned complexion + profound asthenia + nausea + abdominal pain + fever + history of recently discontinued prolonged corticosteroid therapy<\/strong> \u2192 adrenal crisis \u2192 life-threatening emergency \u2192 hydrocortisone 100 mg IV immediate bolus \u2192 NaCl infusion 0.9 % \u2192 glucose IV if hypoglycemia \u2192 hospitalization in intensive care \u2192 decubitus blood pressure figures may be normal but orthostatic fall is major.<\/p>\n <p><strong>Acute hemorrhage + severe orthostatic hypotension + tachycardia + pallor + cold sweat<\/strong> \u2192 onset of hypovolemic shock \u2192 emergency \u2192 IV volemic expansion \u2192 search for hemorrhagic source (hematemesis + melena + post-traumatic hemorrhage + hemoperitoneum) \u2192 transfusion if necessary.<\/p>\n <p><strong>Severe decubitus hypertension (>200\/120 mmHg) discovered in a patient treated with midodrine or fludrocortisone<\/strong> \u2192 iatrogenic decubitus hypertension \u2192 reduce or stop the vesper dose + check that the patient does not take his midodrine in the evening + elevate the head of the bed + MAPA 24h \u2192 urgent reassessment of treatment with the prescribing physician.<\/p>\n <\/div>\n\n <h2>Consult at Clinique Omicron<\/h2>\n <p>Clinique Omicron physicians assess patients presenting with dizziness on rising, repeated falls or orthostatic syncope, perform standardized supine and standing BP measurements, conduct medication review and initiate appropriate non-pharmacological and pharmacological management. Cases of severe HO, progressive neurogenic HO or POTS are referred to specialists in neurology or internal medicine. Consultations are available at several points of service in Quebec, and via telemedicine. To book an appointment, visit <a href=\"https:\/\/cliniqueomicron.ca\">cliniqueomicron.ca<\/a>.<\/p>\n\n <p class=\"co-disclaimer\">The contents of this page are provided for information purposes only and do not replace medical advice. Any fall with loss of consciousness or severe discomfort on rising should be promptly referred to a physician to rule out an urgent cardiac or neurological cause.<\/p>\n<\/div>\n<\/body>\n<\/html>\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t<\/div>","protected":false},"excerpt":{"rendered":"<p>Hypotension orthostatique : causes, diagnostic et traitement | Clinique Omicron Neurologie & M\u00e9decine interne & M\u00e9decine de famille & G\u00e9riatrie Hypotension orthostatique L’hypotension orthostatique (HO) est d\u00e9finie par une chute de la pression art\u00e9rielle systolique (PAS) d’au moins 20 mmHg ou de la pression art\u00e9rielle diastolique (PAD) d’au moins 10 mmHg dans les 3 minutes… <a href=\"https:\/\/cliniqueomicron.ca\/en\/hypotension-orthostatique\/\" rel=\"bookmark\">Read More \"<span class=\"screen-reader-text\">Orthostatic hypotension: causes, diagnosis and treatment | Clinique Omicron<\/span><\/a><\/p>","protected":false},"author":1,"featured_media":0,"parent":0,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"om_disable_all_campaigns":false,"_monsterinsights_skip_tracking":false,"_monsterinsights_sitenote_active":false,"_monsterinsights_sitenote_note":"","_monsterinsights_sitenote_category":0,"neve_meta_sidebar":"","neve_meta_container":"","neve_meta_enable_content_width":"off","neve_meta_content_width":100,"neve_meta_title_alignment":"","neve_meta_author_avatar":"","neve_post_elements_order":"","neve_meta_disable_header":"","neve_meta_disable_footer":"","neve_meta_disable_title":"","_themeisle_gutenberg_block_has_review":false,"_metasync_otto_title":"Hypotension orthostatique : | Brossard | Clinique Omicron","_metasync_otto_description":"L'hypotension orthostatique est une chute de la pression art\u00e9rielle au lever. Causes, bilan \u00e9tiologique, mesures non pharmacologiques, fludrocortisone, midod...","_metasync_otto_keywords":"","_metasync_otto_og_title":"Hypotension orthostatique : | Brossard | Clinique Omicron","_metasync_otto_og_description":"L'hypotension orthostatique est une chute de la pression art\u00e9rielle au lever. Causes, bilan \u00e9tiologique, mesures non pharmacologiques, fludrocortisone, midod...","_metasync_otto_twitter_title":"Hypotension orthostatique : | Brossard | Clinique Omicron","_metasync_otto_twitter_description":"L'hypotension orthostatique est une chute de la pression art\u00e9rielle au lever. 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\n\t\t\t\t\t\n\n\n\n\nOrthostatic hypotension: causes, diagnosis and treatment | Clinique Omicron<\/title>\n<meta name=\"description\" content=\"Orthostatic hypotension is a drop in blood pressure on rising. Causes, etiological assessment, non-pharmacological measures, fludrocortisone, midodrine and management in Quebec.\">\n<meta name=\"keywords\" content=\"hypotension orthostatique traitement, hypotension posturale, chute pression art\u00e9rielle lever, fludrocortisone midodrine, syncope orthostatique, dysautonomie, hypotension orthostatique \u00e2g\u00e9, hypotension orthostatique Qu\u00e9bec\">\n<link rel=\"preconnect\" href=\"https:\/\/fonts.googleapis.com\">\n<link href=\"https:\/\/fonts.googleapis.com\/css2?family=Cinzel:wght@600&family=Poppins:wght@400;500;600;700&display=swap\" rel=\"stylesheet\">\n<style>\n.co-wrap * { font-family: 'Poppins', sans-serif; box-sizing: border-box; }\n.co-wrap { max-width: 1100px; margin: 0 auto; padding: 30px 0 60px; }\n.co-label { font-family: 'Cinzel', serif; font-size: 14px; font-weight: bold; letter-spacing: 1px; text-transform: uppercase; color: #4D6577; margin-bottom: 14px; display: block; }\n.co-wrap h1 { font-size: 32px; font-weight: 500; color: #323C52; margin: 0 0 22px; line-height: 1.2; }\n.co-intro { font-size: 16px; line-height: 1.75; color: #4D6577; margin-bottom: 36px; padding-bottom: 32px; border-bottom: 1px solid rgba(77,101,119,.2); }\n.co-wrap h2 { font-size: 20px; font-weight: 600; color: #323C52; margin: 32px 0 12px; }\n.co-wrap p { font-size: 15px; color: #4D6577; line-height: 1.7; margin-bottom: 14px; }\n.co-list { list-style: none; padding: 0; margin: 12px 0 24px; }\n.co-list li { font-size: 15px; color: #4D6577; padding: 10px 14px 10px 38px; margin-bottom: 8px; border-radius: 6px; position: relative; background: rgba(77,101,119,.06); border-left: 3px solid #4D6577; }\n.co-list li::before { content: \"\u2713\"; position: absolute; left: 12px; font-weight: 700; color: #4D6577; }\n.co-table { width: 100%; border-collapse: collapse; margin: 14px 0 22px; font-size: 14px; border-radius: 8px; overflow: hidden; table-layout: fixed; }\n.co-table thead tr { background: #323C52; color: #fff; }\n.co-table thead th { padding: 11px 16px; text-align: left; font-weight: 600; font-size: 13px; }\n.co-table tbody tr:nth-child(even) { background: rgba(77,101,119,.06); }\n.co-table tbody tr:nth-child(odd) { background: #fff; }\n.co-table td { padding: 10px 16px; color: #4D6577; border-bottom: 1px solid rgba(77,101,119,.12); font-size: 14px; vertical-align: top; }\n.co-table td:first-child { font-weight: 600; color: #323C52; }\n.co-infobox { display: flex; gap: 12px; background: rgba(77,101,119,.06); border-radius: 8px; border-left: 4px solid #4D6577; padding: 14px 18px; margin: 18px 0 28px; font-size: 14px; color: #4D6577; line-height: 1.65; }\n.co-infobox .ico { font-size: 18px; flex-shrink: 0; }\n.co-urgence { background: #fff8f8; border-left: 5px solid #c0392b; border-radius: 6px; padding: 20px 26px; margin: 24px 0 32px; }\n.co-urgence .co-urgence-titre { font-size: 13px; font-weight: 700; color: #c0392b; letter-spacing: 1.5px; text-transform: uppercase; margin-bottom: 10px; }\n.co-urgence p { color: #5a2020; font-size: 14px; margin: 0 0 10px; line-height: 1.7; }\n.co-urgence p:last-child { margin-bottom: 0; }\n.co-disclaimer { font-size: 13px; color: #8a9aaa; font-style: italic; border-top: 1px solid rgba(77,101,119,.15); padding-top: 24px; margin-top: 40px; line-height: 1.6; }\n<\/style>\n<\/head>\n<body>\n<div class=\"co-wrap\">\n <span class=\"co-label\">Neurology & Internal Medicine & Family Medicine & Geriatrics<\/span>\n <h1>Orthostatic hypotension<\/h1>\n\n <div class=\"co-intro\">\n Orthostatic hypotension (OH) is defined as a fall in systolic blood pressure (SBP) of at least 20 mmHg or diastolic blood pressure (DBP) of at least 10 mmHg within 3 minutes of going from lying to standing, with or without symptoms. This consensus definition, established by the European Society of Cardiology and the American Autonomic Society (Freeman 2011 - Journal of the American College of Cardiology), is based on standardized sphygmomanometric measurement. HO results from a maladaptation of the autonomic nervous system and vascular regulatory mechanisms to the gravitational redistribution of blood on rising: normally, the transition to orthostatism results in a venous pooling of 500 to 700 mL in the lower limbs and splanchnic territory, a reduction in venous return and systolic ejection volume, compensated within seconds by sympathetic baroreflex activation (tachycardia + arterial and venous vasoconstriction) and release of noradrenaline, renin and vasopressin. HO occurs when this compensation is insufficient. Its prevalence increases sharply with age - from 5 % before 50 to 30 % after 70 - and represents one of the major causes of falls, syncope, fractures and loss of autonomy in the elderly. HO is also an independent prognostic marker of cardiovascular mortality and cerebrovascular events (Eigenbrodt 2000 - Stroke). In addition to the classic immediate form, there are initial forms (fall within the first minute, often unrecognized because not routinely measured) and delayed forms (after 3-10 minutes), as well as Postural Orthostatic Tachycardia Syndrome (POTS), a distinct entity preferentially affecting young women.\n <\/div>\n\n <h2>Pathophysiology, etiologies and clinical presentation<\/h2>\n <ul class=\"co-list\">\n <li><strong>Mechanisms of normal orthostatic blood pressure regulation and pathophysiology of HO :<\/strong> normal response on rising (chronology): 0-30 seconds: venous pooling \u2192 reduction in venous return \u2192 drop in ejection volume (-40 %) \u2192 transient fall in BP \u2192 immediate activation of carotid and aortic baroreceptors \u2192 reflex sympathetic discharge \u2192 tachycardia (HR +10-25 bpm) + arteriolar and venous vasoconstriction \u2192 30 seconds - 2 minutes: noradrenalin secretion + RAAS activation (renin \u2192 angiotensin II \u2192 aldosterone) + vasopressin (ADH) \u2192 consolidation of vasoconstriction + 2-10 minutes: complete normalization of BP \u2192 prolonged standing \u2192 active calf muscle mechanisms (venous muscle pump); pathophysiology of HO: baroreceptor reflex arc defect (most common): damage to efferent sympathetic fibers (autonomic neuropathy) \u2192 no adequate vasoconstriction \u2192 uncompensated fall in BP \u2192 in diabetic neuropathy + amyloidosis + multisystem atrophy (MSA) + Parkinson's disease \u2192 absolute hypovolemia: reduction in circulating blood volume \u2192 insufficient supply to the baroreflex \u2192 dehydration + adrenal insufficiency + hemorrhage + drug causes: drugs are the leading cause of acquired HO in clinical practice \u2192 alpha-adrenergic blockade (alpha-blockers + antipsychotics) \u2192 baroreflex blockade (beta-blockers) \u2192 volume reduction (diuretics) \u2192 direct vasodilation (nitrate derivatives + ACE inhibitors + calcium antagonists) \u2192 other mechanisms; specific features of HO in the elderly: less sensitive baroreflex (less compliant arteries) + reduced renal response to aldosterone + decreased thirst \u2192 tendency to chronic hypovolemia + polypharmacy + multiple comorbidities \u2192 HO in 30 % of institutionalized elderly (Rutan 1992 - Hypertension) \u2192 association HO + risk of falling \u00d7 2.6 (Gangavati 2011 - Archives of Internal Medicine) \u2192 mortality: Eigenbrodt 2000 - Stroke: HO \u2192 risk of stroke \u00d7 2.0 + risk of death \u00d7 1.36 over 10 years \u2192 postprandial orthostatic hypotension: worsening of HO in the 60-90 min following a meal \u2192 uncompensated postprandial mesenteric vasodilation \u2192 frequent in the elderly + Parkinson + dysautonomia \u2192 light + small + fractionated meals \u2192 avoid alcohol with meals<\/li>\n <li><strong>Etiological classification - neurogenic, drug-induced and systemic causes :<\/strong> Neurogenic HO (dysautonomia) - most severe and hardest to treat: primary dysautonomias - degenerative: multisystem atrophy (MSA): synucleinopathy \u2192 degeneration of preganglionic sympathetic neurons of the vasomotor center \u2192 severe HO + Parkinson's (OH in 20-50 %) + dementia with Lewy bodies (DCL) + pure Parkinson's disease \u2192 secondary dysautonomias (autonomic neuropathies): diabetes (diabetic autonomic neuropathy - 25-30 % of type 1 diabetics + 15-20 % of type 2) \u2192 most frequent form of secondary dysautonomia \u2192 amyloidosis (AL + transthyretin) \u2192 accumulation of amyloid fibrils in autonomic nerves + vessels \u2192 severe HO \u2192 HIV \u2192 paraneoplastic syndromes (anti-HU + anti-VGCC + anti-ganglial - autoimmune autonomic ganglionopathy) \u2192 chronic alcoholism \u2192 rare infiltrative diseases (sarcoidosis + leprosy) ; drug-induced causes (leading cause of acquired HO in practice): diuretics (thiazides + furosemide) \u2192 hypovolemia \u2192 alpha-blockers (tamsulosin + doxazosin + alfuzosin) \u2192 arteriolar vasodilation \u2192 HO ++ \u2192 central antihypertensives (clonidine + methyldopa) \u2192 central sympathetic inhibition \u2192 antipsychotics (risperidone + haloperidol + chlorpromazine + olanzapine) \u2192 alpha blockade1 + anticholinergic \u2192 HO ++ \u2192 tricyclic antidepressants (imipramine + amitriptyline) \u2192 alpha-blockade1 + anticholinergic \u2192 MAOI \u2192 noradrenaline depletion + nitrate derivatives (nitroglycerin + isosorbide) \u2192 massive venous vasodilation \u2192 calcium-channel blockers (amlodipine + nifedipine) + ACEI\/ARA-2 \u2192 vasodilation \u2192 worsening of HO \u2192 levodopa + dopaminergic agonists (pramipexole + ropinirole) in Parkinson \u2192 vasodilation + sympathetic inhibition \u2192 opioids \u2192 sympathetic inhibition + vasodilation \u2192 anesthetics (spinal anesthesia + epidural + general agents) ; non-drug systemic causes: dehydration (very frequent causes): gastroenteritis + diaphoresis + insufficient intake \u2192 adrenal insufficiency (adrenal crisis): low cortisol \u2192 insufficient RAAS + reduced vascular response \u2192 severe HO + hyponatremia + abdominal pain \u2192 emergency \u2192 acute hemorrhage \u2192 absolute hypovolemia \u2192 cardiac insufficiency (reduced output) \u2192 venous causes: major varicose veins + prolonged bed rest (deconditioning + reduced plasma volume) + pregnancy (vasodilation + compression cave) + POTS (postural orthostatic tachycardia syndrome) : entity distinct from HO \u2192 tachycardia \u226530 bpm on rising (or HR \u2265120 bpm) without significant BP drop \u2192 young women (15-50 years) \u2192 pathophysiology: relative hypovolemia + distal autonomic neuropathy + compensatory sympathetic hyperactivity \u2192 post-COVID: marked increase in POTS cases since 2020 (Taub 2022 - Nature Reviews Cardiology)<\/li>\n <li><strong>Clinical presentation, standardized measurements and additional tests :<\/strong> HO symptoms : classically within the first 3 minutes of rising \u2192 lipothymia (sensation of impending malaise + blurred vision + vertigo) + pre-syncope (dizziness + instability) + syncope (brief loss of consciousness) + tunnel vision + tinnitus + occipital headache (\u00abcoat hanger headache\u00bb - pain in a hanger over the neck and shoulders \u2192 insufficient irrigation of the paravertebral muscles by the vertebral artery) + generalized weakness + falling + nausea \u2192 asymptomatic HO: documented BP drop without symptoms \u2192 frequent \u2192 prognosis less favorable than no HO but fewer immediate falls; standardized measurement of orthostatic BP (ESC 2018 + Freeman 2011 JACC): strict supine \u22655 minutes \u2192 measure BP supine \u2192 stand up active \u2192 measure BP at 1 min + 3 min orthostatically (and at 5 min if available) \u2192 take HR into account at each measurement \u2192 HO confirmed if: PAS fall \u226520 mmHg or PAD \u226510 mmHg within 3 min \u2192 initial (early) HO: fall \u226540 mmHg within the first 15-30 seconds \u2192 not documented by measurement at 1 min \u2192 requires continuous BP monitoring (Finapres + Task Force Monitor) \u2192 delayed (delayed) HO: fall \u226520\/10 mmHg appearing after 3 minutes of rising \u2192 documented by measurement at 5-10 min \u2192 often in elderly subjects with mild neurogenic HO \u2192 tilt test (tilt table): measurement of BP and HR in supine position + tilt at 60-70\u00b0 for 20-45 min \u2192 documented continuous BP + HR \u2192 diagnosis of hard-to-detect forms of HO + vasovagal syncope (syncope within the first 20 minutes on tilt-test) + POTS (tachycardia \u226530 bpm without syncope); targeted etiological workup according to clinic: CBC (anemia) + ionogram + creatinine (eGFR) + glycemia + HbA1c (diabetes) + morning cortisol (adrenal insufficiency) + TSH (hypothyroidism + hyperthyroidism) + renal workup + proteinuria (amyloidosis) + plasma catecholamine assay, supine and standing + plasma norepinephrine assay, supine and standing (in specialized center): noradrenaline not rising on rising \u2192 peripheral dysautonomia (AMS type P or Parkinson) vs excessive rise \u2192 compensatory sympathetic hyperactivity \u2192 ECG + Holter: arrhythmias causing syncope \u2192 24h ambulatory pressure Holter (ABPM): assessment of nocturnal blood pressure profile (nocturnal hypertension often associated with HO in dysautonomias) \u2192 sweating test + Valsalva reflex (in autonomic laboratory) + cerebral MRI if associated neurological signs <\/ul>\n\n <h2>Management - non-pharmacological measures and treatments<\/h2>\n <table class=\"co-table\">\n <colgroup><col style=\"width:200px;\"><col style=\"width:42%;\"><col><\/colgroup>\n <thead>\n <tr><th>Treatment \/ intervention<\/th><th>Mechanism and practical details<\/th><th>Evidence and follow-up<\/th><\/tr>\n <\/thead>\n <tbody>\n <tr>\n <td>Non-pharmacological measures - Universal 1st line<br><small style=\"font-weight:400;color:#7a8fa0;\">Hydration - salt - counter-pressure - gradual rising - split meals - compression stockings<\/small><\/td>\n <td>Behavioral measures and patient education - ESC 2018 + AAN (American Academy of Neurology) 2017 recommendations: sufficient hydration: target 2-2.5 L\/d of fluids \u2192 water, broths, juices \u2192 rapid correction of hypovolemic HO \u2192 hydration bolus of 500 mL of cold water ingested rapidly (over 2-5 min) \u2192 increase in systolic BP of 20-35 mmHg over 20-30 min \u2192 mechanism: orthostatic reflex via osmostimulation of the gastrointestinal tract \u2192 useful in anticipated HO situations (meals + early rising) \u2192 Jordan 2000 - Circulation: demonstration of the pressor reflex of ingested water + increased sodium intake: dietary salt 6-10 g\/d (vs. 5-6 g recommended in HTA) \u2192 increases blood volume \u2192 BUT contraindicated if IC + severe HTA + advanced CKD \u2192 NaCl tablets 1 g \u00d7 3\/d alternatively if insufficient nutrition; physical counterpressure maneuvers (PCM): leg crossing + isometric contraction of leg and gluteal muscles + squat (squatting briefly) + pumping feet alternately \u2192 mechanism: compression of lower limb veins \u2192 reduction in venous pooling \u2192 increase in venous return \u2192 increase in BP by 10-30 mmHg \u2192 van Lieshout 2000 - Journal of Applied Physiology: PCM \u2192 increase in systolic BP +20 mmHg \u2192 Brignole 2004 - Journal of the American College of Cardiology: PCM \u2192 reduction in vasovagal syncope in the PC-Trial; progressive rising and behavioral education: get up in 3 stages (sitting position at the edge of the bed \u2192 wait 30-60 seconds with feet on the floor \u2192 get up) + avoid rapid nocturnal getting up (greatest vulnerability is in the morning when getting up after a night) + avoid hot environments (heat \u2192 cutaneous vasodilation \u2192 worsens HO) + avoid alcohol (vasodilation + inhibition of the baroreflex) + avoid intense exertion on an empty stomach + compression stockings and compressive clothing: class II-III compression stockings (30-40 mmHg) up to the thigh \u2192 reduce venous pooling in the lower limbs \u2192 effective if worn early in the morning (before getting up if possible) \u2192 modest effectiveness in practice (often poor tolerance in the elderly) + abdominal binder: compression of splanchnic territory \u2192 complementary mechanism \u2192 can be combined with compression stockings \u2192 more tolerated than stockings \u2192 Smit 2004 - Journal of Neurology Neurosurgery and Psychiatry: stockings + belt \u2192 12 mmHg BP improvement + elevation of head of bed (30\u00b0): counterintuitive but effective in severe dysautonomia \u2192 reduces nocturnal diuresis + improves plasma volume \u2192 must be associated with raised head of bed (no tilting of whole mattress) \u2192 fractionated and small meals: postprandial HO \u2192 5-6 small meals\/d vs 3 large \u2192 reduced carbohydrate load per meal \u2192 coffee or caffeine before meals: vasoconstriction + pressor effect \u2192 200-250 mg (1-2 cups) before main meal \u2192 effective in postprandial HO<\/td>\n <td>Medication review - key step often undervalued: systematically review ALL the patient's medications before initiating pharmacological treatment of HO \u2192 medications to be reduced or stopped as a priority: diuretics (furosemide + hydrochlorothiazide + indapamide) \u2192 reduce or stop if symptomatic HO \u2192 particularly in the elderly patient + alpha-blockers (tamsulosin + alfuzosin + doxazosin) \u2192 BPH \u2192 alternatives: 5-ARI inhibitors (finasteride) + centrally acting dual antihypertensives (clonidine + methyldopa) \u2192 less hypotensive alternatives + tricyclic antidepressants \u2192 alternatives: SSRIs (less hypotensive) + beta-blockers + calcium channel blockers \u2192 reassess indication and dose + nitrates \u2192 use only on demand if possible + opioid analgesics \u2192 reduce if possible + assess benefit-risk balance; 24h ABPM to detect associated nocturnal hypertension: patients with severe dysautonomia (AMS + Parkinson + diabetic neuropathy) often present paradoxical nocturnal hypertension (reverse dipping) \u2192 elevated nocturnal BP \u2192 risk of nocturnal stroke \u2192 nocturnal diuretics sometimes indicated despite diurnal HO \u2192 complex management \u2192 autonomic specialist \u2192 elevation of head of bed \u2192 reduces nocturnal pressure + improves diurnal HO (renal aldosterone mechanism); exercise and reconditioning: pool exercise (aquatherapy): horizontal positioning + hydrostatic pressure \u2192 maintains plasma volume \u2192 avoids orthostatic drop during exercise + recumbent or supine bike exercise \u2192 avoid standing until sufficient conditioning + progressive orthostatic training (tilt training) \u2192 improves baroreflex sensitivity + venous deconditioning \u2192 useful in POTS + lower limb strengthening exercise \u2192 improves venous muscle pumping<\/td>\n <\/tr>\n <tr>\n <td>Fludrocortisone - mineralocorticoid<br><small style=\"font-weight:400;color:#7a8fa0;\">Volume expansion - 0.1-0.3 mg\/d - hypokalemia - edema - nocturnal hypertension<\/small><\/td>\n <td>Fludrocortisone mechanism of action: synthetic aldosterone analog \u2192 strong mineralocorticoid effect (300\u00d7 endogenous aldosterone) \u2192 weak glucocorticoid effect \u2192 binding to mineralocorticoid receptor in collecting tubule \u2192 Na\u207a reabsorption + K\u207a excretion \u2192 plasma volume expansion \u2192 increased venous return \u2192 improved orthostatic BP \u2192 beneficial accessory effects: sensitization of vascular alpha-adrenergic receptors to noradrenaline \u2192 improvement of reflex vasoconstriction \u2192 dosage: 0.05-0.3 mg\/d po \u2192 start at 0.05-0.1 mg\/d \u2192 gradual increase every 1-2 weeks depending on response and tolerance \u2192 maximum effect expected at 1-2 weeks \u2192 usual maximum dose: 0.3-0.4 mg\/d (beyond that \u2192 significant side effects with no additional benefit) \u2192 taken in the morning (to minimize nocturnal hypertension); preferred indications: neurogenic dysautonomia (AMS + autonomic neuropathy + Parkinson + relative adrenal insufficiency) \u2192 relative hypovolemic HO (POTS + deconditioning) \u2192 efficacy in clinical trials: Logan 1966 - Circulation: first trials showing efficacy in dysautonomia + meta-analyses and systematic reviews (Figueroa 2010 - Clinical Autonomic Research): fludrocortisone \u2192 improvement in orthostatic BP + reduction in symptoms + moderate level of evidence (few large randomized trials) \u2192 CHSA Trial (Lahrmann 2006 - Movement Disorders): fludrocortisone + domperidone in AMS \u2192 modest improvement \u2192 main side effects: hypokalemia (monitor kalemia + K\u207a supplementation if <3.5 mmol\/L) + fluid retention \u2192 peripheral edema + decubitus hypertension (nocturnal hypertension) \u2192 special attention in patients with mild IC \u2192 worsening of heart failure \u2192 relative contraindications: decompensated heart failure + severe CKD (eGFR <30) + severe uncontrolled hypertension + pre-existing hypokalemia \u2192 biological monitoring: kalemia + creatinine + supine and standing BP \u2192 at 2 weeks + 1 month + 3 months + then quarterly<\/td>\n <td>Comparative efficacy and place in therapeutic strategy: fludrocortisone is often considered the 1st-line agent in severe dysautonomias despite a moderate level of evidence \u2192 its benefit is best documented in adrenal insufficiency (formal indication) + in primary neurogenic dysautonomias \u2192 in drug-induced or hypovolemic HO \u2192 etiological treatment as a priority \u2192 fludrocortisone as temporary support if necessary \u2192 in POTS \u2192 fludrocortisone effective in increasing blood volume \u2192 but may worsen reflex tachycardia \u2192 combine with low-dose beta-blockers (propranolol 10-20 mg) in POTS \u2192 CHAMP trial (Taub 2021 - NEJM : pediatric randomized trial) \u2192 in pediatric POTS: propranolol + fludrocortisone \u2192 both superior to placebo on symptoms + ivabradine as an alternative if beta blockers poorly tolerated in POTS \u2192 frequently used combinations: fludrocortisone + midodrine (synergistic benefit on standing BP) + fludrocortisone + pyridostigmine + droxidopa in AMS \u2192 polypharmacy necessary in severe forms<\/td>\n <\/tr>\n <tr>\n <td>Midodrine - alpha-1 adrenergic agonist<br><small style=\"font-weight:400;color:#7a8fa0;\">Vasoconstriction - 2.5-10 mg \u00d7 3\/d - decubitus hypertension - urinary retention - piloerection<\/small><\/td>\n <td>Mechanism and pharmacological profile of midodrine: direct alpha-1 adrenergic receptor agonist \u2192 peripheral arteriolar and venous vasoconstriction \u2192 increased peripheral vascular resistance \u2192 increased BP \u2192 prodrug: metabolized to desglymidodrine (active metabolite) \u2192 half-life: 2-3h \u2192 maximum effect 1h after intake \u2192 duration of action: 3-4h \u2192 does not cross the blood-brain barrier (advantage: no central effects) \u2192 no direct cardiac action (no tachycardia); dosage and administration: start at 2.5 mg \u00d7 2\/d \u2192 increase to 2.5-10 mg \u00d7 3\/d according to response and tolerance \u2192 intakes: morning + midday + late afternoon \u2192 NEVER take late evening or at bedtime (risk of severe nocturnal decubitus hypertension) \u2192 avoid in the 4h preceding bedtime \u2192 take 15-30 min before risk situations (getting up + eating) \u2192 FDA 1996 approval (Mathias 1995 - Lancet : randomized trial \u2192 midodrine \u00d7 4 weeks \u2192 improvement in orthostatic BP and symptoms) \u2192 Health Canada approval \u2192 RAMQ reimbursement (exception drug or regular list depending on formulation) \u2192 clinical efficacy: Jankovic 1993 - Neurology + Wright 1998 - JAMA Internal Medicine: midodrine \u2192 improvement in orthostatic BP +22 mmHg (systolic) vs placebo \u2192 improvement in symptoms (lipothymia + dizziness + syncope) \u2192 non-inferiority trial vs fludrocortisone \u2192 comparable with different safety profile; contraindications to midodrine: severe hypertension (systolic BP >180 mmHg at rest) + heart failure \u2192 worsening preload + significant urinary retention (urethral alpha-1 agonist \u2192 urethral sphincter contraction) + pheochromocytoma + hyperthyroidism + severe coronary disease + severe renal insufficiency (accumulation)<\/td>\n <td>Midodrine side effects and clinical management: decubitus hypertension (supine hypertension): pressor effect persists in supine position \u2192 significant + sometimes severe hypertension \u2192 main limiting side effect \u2192 absolute rule: never take before bedtime + always measure supine BP before each prescription \u2192 if nocturnal hypertension \u2192 reduce afternoon dose + elevate head of bed + piloerection (goose bumps) + scalp itching : alpha-1 effect on hair erector muscles \u2192 frequent + benign \u2192 may alert patient to drug efficacy + urinary retention: urethral alpha-1 effects + caution if BPH + check RPM if urinary symptoms + paresthesias + cold sensation of extremities (excessive vasoconstriction) \u2192 reduce dose + mild reflex bradycardia: vasoconstriction \u2192 slight increase in resistances \u2192 reflex decrease in HR \u2192 rare but watch for BAV; therapeutic associations and combinations in severe HO: midodrine + fludrocortisone \u2192 most frequent combination in SMA and severe dysautonomias \u2192 synergistic benefit (increased blood volume + vasoconstriction) \u2192 midodrine + pyridostigmine \u2192 pyridostigmine (acetylcholinesterase inhibitor) \u2192 increases sympathetic tone via the autonomic nervous system \u2192 Sandroni 2006 - Clinical Pharmacology and Therapeutics : pyridostigmine 30-60 mg \u00d7 3\/d \u2192 improvement of neurogenic HO without worsening nocturnal HTA (major advantage vs fludrocortisone) \u2192 midodrine + droxidopa (in AMS and Parkinson's disease) \u2192 triple combination in the most severe forms<\/td>\n <\/tr>\n <tr>\n <td>Droxidopa and other agents - AMS, Parkinson, POTS<br><small style=\"font-weight:400;color:#7a8fa0;\">Droxidopa - pyridostigmine - octreotide - erythropoietin - beta-blockers POTS<\/small><\/td>\n <td>Droxidopa (Northera) - noradrenaline precursor: mechanism: oral noradrenaline precursor \u2192 converted by DOPA decarboxylase into noradrenaline \u2192 acts directly on peripheral and central adrenergic receptors \u2192 restores noradrenaline levels in sympathetic synapses \u2192 specifically indicated in dysautonomias with noradrenaline depletion : dopamine beta-hydroxylase deficiency (DBH - very rare) + AMS + pure autonomic failure (PAF) + Parkinson's with refractory HO \u2192 FDA 2014 approval (ADAPT study - Kaufmann 2014 - New England Journal of Medicine : droxidopa \u2192 improvement of HO symptoms and orthostatic BP in neurogenic HO) \u2192 not available in RAMQ drug list at time of data - check current availability \u2192 dosage: 100 mg \u00d7 3\/d \u2192 titration up to 600 mg \u00d7 3\/d \u2192 side effects: decubitus hypertension + headache + nausea + fatigue; pyridostigmine (Mestinon): acetylcholinesterase inhibitor \u2192 increases acetylcholine in autonomic synapses \u2192 potentiates reflex sympathetic tone via autonomic ganglia \u2192 unique advantage: improves standing HO WITHOUT significantly worsening supine BP \u2192 unlike midodrine and fludrocortisone \u2192 Singer 2006 - Annals of Internal Medicine: pyridostigmine 30-60 mg \u00d7 3\/d \u2192 improves standing BP without nocturnal hypertension \u2192 indication: neurogenic HO with associated nocturnal hypertension (situation where midodrine and fludrocortisone are difficult to use) + side effects: diarrhea + abdominal cramps + hypersalivation + bronchospasm (caution if asthma\/BPCO) + fasciculations \u2192 dosage: 30 mg \u00d7 3\/d \u2192 up to 60 mg \u00d7 3\/d; octreotide (long-acting somatostatin): inhibits postprandial mesenteric vasodilation + inhibits release of intestinal vasodilatory peptides \u2192 indicated specifically in refractory postprandial HO \u2192 25-50 \u00b5g SC before meals \u2192 disadvantage: subcutaneous route + digestive effects (nausea + biliary lithiasis); recombinant erythropoietin (EPO): stimulates erythropoiesis \u2192 increases total blood volume \u2192 useful in HO associated with anemia + in AMS and pure autonomic failure with mild anemia \u2192 little robust data + high cost; POTS - specific treatment: low-dose beta-blockers (propranolol 10-20 mg) \u2192 reduce reflex tachycardia without further lowering BP + ivabradine (5 mg \u00d7 2\/d - off MA): If inhibitor \u2192 reduces tachycardia without vascular effect \u2192 Barzilai 2019 - European Heart Journal Case Reports + treatment of cause: post-COVID autonomic neuropathy \u2192 fludrocortisone + reconditioning + compression<\/td>\n <td>Management of nocturnal hypertension in patients with diurnal HO - therapeutic paradox: frequent problem in severe dysautonomias: severe diurnal HO + nocturnal HTA (reverse dipping) \u2192 risk of nocturnal stroke \u2192 difficult to treat simultaneously \u2192 strategies: elevation of head of bed to 30\u00b0 \u2192 reduces nocturnal HTA (renal redistribution of blood + reduced filtration pressure) \u2192 improves diurnal HO (maintenance of plasma volume) \u2192 most effective measure for both components + nocturnal nitroglycerin patch (0.1-0,2 mg\/h) \u2192 if severe nocturnal HTA \u2192 to be removed in the morning \u2192 mineralocorticoid receptor antagonist (losartan) in the evening \u2192 reduction of nocturnal HTA without worsening morning HO \u2192 Omboni 2006 - Hypertension + pyridostigmine (does not cause nocturnal HTA) \u2192 advantage over midodrine + fludrocortisone \u2192 change timing of midodrine doses (avoid late afternoon dose) ; long-term monitoring and follow-up of HO: 24h ABPM: every 6-12 months \u2192 nocturnal profile assessment + falls score (Morse + Tinetti) + autonomy assessment \u2192 symptom diary (frequency of lipothymia + syncope + falls) \u2192 neurological reassessment if progressive HO (AMS + Parkinson's) \u2192 adaptation of technical aids (cane + walker + lift chair) \u2192 caregiver education + home occupational therapy (securing the environment + mats + grab bars)<\/td>\n <\/tr>\n <\/tbody>\n <\/table>\n\n <div class=\"co-infobox\">\n <span class=\"ico\">\u2139\ufe0f<\/span>\n <span><strong>Medication revision is the first step in treating orthostatic hypotension:<\/strong> drugs - diuretics, alpha-blockers, central antihypertensives, antipsychotics, tricyclic antidepressants, nitrates, opioids - represent the leading cause of acquired HO in clinical practice. Before adding pharmacological treatment to HO, it is essential to identify and reduce or stop non-essential hypotensive drugs, particularly in elderly patients on polymedication. Even a modest reduction in dose can eliminate HO without the need to add a new drug.<\/span>\n <\/div>\n\n <div class=\"co-urgence\">\n <div class=\"co-urgence-titre\">Situations requiring urgent medical assessment<\/div>\n <p><strong>Syncope on rising + head trauma + high-kinetic fall (suspected hip fracture) + prolonged loss of consciousness (>1-2 minutes) + persistent post-syncope confusion<\/strong> \u2192 call 911 + emergency room assessment \u2192 cranial CT scan if trauma + hip X-ray + etiological assessment of syncope \u2192 ECG + cardiac monitoring \u2192 do not leave patient alone until medical assessment.<\/p>\n <p><strong>HO severe + hyponatremia + hyperkalemia + tanned complexion + profound asthenia + nausea + abdominal pain + fever + history of recently discontinued prolonged corticosteroid therapy<\/strong> \u2192 adrenal crisis \u2192 life-threatening emergency \u2192 hydrocortisone 100 mg IV immediate bolus \u2192 NaCl infusion 0.9 % \u2192 glucose IV if hypoglycemia \u2192 hospitalization in intensive care \u2192 decubitus blood pressure figures may be normal but orthostatic fall is major.<\/p>\n <p><strong>Acute hemorrhage + severe orthostatic hypotension + tachycardia + pallor + cold sweat<\/strong> \u2192 onset of hypovolemic shock \u2192 emergency \u2192 IV volemic expansion \u2192 search for hemorrhagic source (hematemesis + melena + post-traumatic hemorrhage + hemoperitoneum) \u2192 transfusion if necessary.<\/p>\n <p><strong>Severe decubitus hypertension (>200\/120 mmHg) discovered in a patient treated with midodrine or fludrocortisone<\/strong> \u2192 iatrogenic decubitus hypertension \u2192 reduce or stop the vesper dose + check that the patient does not take his midodrine in the evening + elevate the head of the bed + MAPA 24h \u2192 urgent reassessment of treatment with the prescribing physician.<\/p>\n <\/div>\n\n <h2>Consult at Clinique Omicron<\/h2>\n <p>Clinique Omicron physicians assess patients presenting with dizziness on rising, repeated falls or orthostatic syncope, perform standardized supine and standing BP measurements, conduct medication review and initiate appropriate non-pharmacological and pharmacological management. Cases of severe HO, progressive neurogenic HO or POTS are referred to specialists in neurology or internal medicine. Consultations are available at several points of service in Quebec, and via telemedicine. To book an appointment, visit <a href=\"https:\/\/cliniqueomicron.ca\">cliniqueomicron.ca<\/a>.<\/p>\n\n <p class=\"co-disclaimer\">The contents of this page are provided for information purposes only and do not replace medical advice. Any fall with loss of consciousness or severe discomfort on rising should be promptly referred to a physician to rule out an urgent cardiac or neurological cause.<\/p>\n<\/div>\n<\/body>\n<\/html>\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t<\/div>","protected":false},"excerpt":{"rendered":"<p>Hypotension orthostatique : causes, diagnostic et traitement | Clinique Omicron Neurologie & M\u00e9decine interne & M\u00e9decine de famille & G\u00e9riatrie Hypotension orthostatique L’hypotension orthostatique (HO) est d\u00e9finie par une chute de la pression art\u00e9rielle systolique (PAS) d’au moins 20 mmHg ou de la pression art\u00e9rielle diastolique (PAD) d’au moins 10 mmHg dans les 3 minutes… <a href=\"https:\/\/cliniqueomicron.ca\/en\/hypotension-orthostatique\/\" rel=\"bookmark\">Read More \"<span class=\"screen-reader-text\">Orthostatic hypotension: causes, diagnosis and treatment | Clinique Omicron<\/span><\/a><\/p>","protected":false},"author":1,"featured_media":0,"parent":0,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"om_disable_all_campaigns":false,"_monsterinsights_skip_tracking":false,"_monsterinsights_sitenote_active":false,"_monsterinsights_sitenote_note":"","_monsterinsights_sitenote_category":0,"neve_meta_sidebar":"","neve_meta_container":"","neve_meta_enable_content_width":"off","neve_meta_content_width":100,"neve_meta_title_alignment":"","neve_meta_author_avatar":"","neve_post_elements_order":"","neve_meta_disable_header":"","neve_meta_disable_footer":"","neve_meta_disable_title":"","_themeisle_gutenberg_block_has_review":false,"_metasync_otto_title":"Hypotension orthostatique : | Brossard | Clinique Omicron","_metasync_otto_description":"L'hypotension orthostatique est une chute de la pression art\u00e9rielle au lever. Causes, bilan \u00e9tiologique, mesures non pharmacologiques, fludrocortisone, midod...","_metasync_otto_keywords":"","_metasync_otto_og_title":"Hypotension orthostatique : | Brossard | Clinique Omicron","_metasync_otto_og_description":"L'hypotension orthostatique est une chute de la pression art\u00e9rielle au lever. Causes, bilan \u00e9tiologique, mesures non pharmacologiques, fludrocortisone, midod...","_metasync_otto_twitter_title":"Hypotension orthostatique : | Brossard | Clinique Omicron","_metasync_otto_twitter_description":"L'hypotension orthostatique est une chute de la pression art\u00e9rielle au lever. Causes, bilan \u00e9tiologique, mesures non pharmacologiques, fludrocortisone, midod...","rank_math_title":"","rank_math_description":"","_yoast_wpseo_title":"","_yoast_wpseo_metadesc":"","_aioseo_title":"Hypotension orthostatique : causes, diagnostic et traitement | Clinique Omicron","_aioseo_description":"L'hypotension orthostatique est une chute de la pression art\u00e9rielle au lever. Causes, bilan \u00e9tiologique, mesures non pharmacologiques, fludrocortisone, midodrine et prise en charge au Qu\u00e9bec.","_metasync_seo_title":"","_metasync_seo_desc":"","_metasync_breadcrumb_title":"","_metasync_primary_category":0,"_metasync_primary_product_cat":0,"_metasync_otto_disabled":"","_metasync_hreflang":"","_metasync_plugin_sync_ts":"{\"aioseo\":\"2026-05-04T21:51:37+00:00\"}","_metasync_robots_advanced":"","footnotes":""},"class_list":["post-24684","page","type-page","status-publish","hentry"],"aioseo_notices":[],"_links":{"self":[{"href":"https:\/\/cliniqueomicron.ca\/en\/wp-json\/wp\/v2\/pages\/24684","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/cliniqueomicron.ca\/en\/wp-json\/wp\/v2\/pages"}],"about":[{"href":"https:\/\/cliniqueomicron.ca\/en\/wp-json\/wp\/v2\/types\/page"}],"author":[{"embeddable":true,"href":"https:\/\/cliniqueomicron.ca\/en\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/cliniqueomicron.ca\/en\/wp-json\/wp\/v2\/comments?post=24684"}],"version-history":[{"count":4,"href":"https:\/\/cliniqueomicron.ca\/en\/wp-json\/wp\/v2\/pages\/24684\/revisions"}],"predecessor-version":[{"id":29614,"href":"https:\/\/cliniqueomicron.ca\/en\/wp-json\/wp\/v2\/pages\/24684\/revisions\/29614"}],"wp:attachment":[{"href":"https:\/\/cliniqueomicron.ca\/en\/wp-json\/wp\/v2\/media?parent=24684"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}