01Approach to the Critical Patient/attcp47

Immediate stabilization

›Airway and perfusion assessment

›Patient unresponsive or altered: position supine, elevate legs

›Cardiac monitor and continuous pulse oximetry

›IV access with large-bore peripheral line

›Persistent SBP <90 mmHg after lying flat

›IV isotonic saline 500 mL bolus over 15 minutes

›Repeat orthostatic vitals after initial fluid

›SpO2 <92% or cyanosis

›Supplemental oxygen to maintain SpO2 >=94%

›Rule out concurrent PE or cardiac event

High-risk features requiring urgent workup

›Cardiac cannot-miss triggers

›Syncope during exertion

›Immediate 12-lead ECG

›Cardiology consult for structural etiology

›Syncope while supine or without prodrome

›Arrhythmia evaluation with monitoring

›Extended telemetry if available

›Associated chest pain or palpitations

›Troponin and BNP

›Echocardiography if new murmur

›Neurologic cannot-miss triggers

›Focal deficit, dysarthria, or facial droop

›Stroke protocol activation

›CT head non-contrast emergent

›Prolonged LOC or postictal confusion >5 minutes

›Seizure evaluation

02History/hx86

Presentation pattern

›Core syncopal event details

›Positional trigger: standing from supine or sitting

›Onset within 3 minutes of standing (classic OH)

›Onset beyond 3 minutes (delayed OH)

›Prodrome symptoms

›Lightheadedness or presyncope

›Visual dimming or tunnel vision

›Muffled hearing or cognitive slowing

›Warmth, diaphoresis, or nausea

›Duration of LOC

›Brief seconds (typical for OH)

›>1 minute: consider cardiac or seizure

›Recovery pattern

›Immediate improvement on lying down (typical OH)

›Prolonged confusion: seizure or cardiac

Timing and triggers

›Situational context

›Morning episodes: post-overnight natriuresis

›First stand of the day

›After prolonged recumbency

›Postprandial timing: within 15-90 minutes of meals

›Carbohydrate-heavy meal worsens splanchnic pooling

›Post-exertion: within minutes of stopping exercise

›Venous pooling in lower extremities

›Environmental triggers

›Hot environment or hot shower/bath

›Prolonged standing (>5 minutes)

›Alcohol ingestion

Medication history

›Offending agents

›Antihypertensives

›Alpha-blockers (doxazosin, prazosin, tamsulosin)

›Calcium channel blockers

›ACE inhibitors and ARBs

›Volume-depleting agents

›Loop diuretics (furosemide, bumetanide)

›Thiazide diuretics

›Nitrates and vasodilators

›Neurologically active agents

›Levodopa and dopamine agonists

›Tricyclic antidepressants and MAOIs

›Antipsychotics (phenothiazines, atypicals)

›Opioids and benzodiazepines

›PDE5 inhibitors (sildenafil, tadalafil)

›Recent medication changes

›New prescription within 2 weeks

›Dose escalation

Alarm features

›High-risk history elements

›Exertional syncope or syncope while supine

›Cardiac etiology until proven otherwise

›Palpitations immediately before LOC

›Ventricular tachycardia concern

›Chest pain or dyspnea associated

›PE, ACS, aortic stenosis consideration

›Family history of sudden cardiac death

›Channelopathy (long QT, Brugada) workup

›GI bleeding signs

›Melena, hematemesis, hematochezia

›Significant anemia as cause

›"Coat hanger" neck and shoulder pain

›Highly specific for neurogenic OH

Review of systems

›Autonomic and neurologic symptoms

›Tremor, rigidity, or gait instability

›Parkinson disease or synucleinopathy

›Urinary retention or incontinence

›Autonomic neuropathy marker

›Erectile dysfunction

›Peripheral autonomic involvement

›Constipation or gastroparesis symptoms

›GI autonomic dysfunction

›Constitutional and endocrine

›Polyuria or polydipsia: diabetes mellitus

›Fatigue and weight loss: adrenal insufficiency

›Nausea, vomiting, diarrhea: volume depletion

Risk factors

›Patient-level risk

›Age >60-70 years

›Impaired baroreflex sensitivity

›Reduced plasma volume conservation

›Polypharmacy (>=4 medications)

›Neurodegenerative disease

›Parkinson disease

›Multiple system atrophy

›Dementia with Lewy bodies

›Diabetes mellitus

›Autonomic neuropathy in up to 30% with long-standing disease

›Deconditioning or prolonged bed rest

›Frailty and sarcopenia

›Supine hypertension coexisting with nOH (~50% of patients)

03Physical Exam/exam72

Orthostatic vital signs

›Standard measurement protocol

›Supine rest for 5 minutes before standing

›Baseline SBP, DBP, and HR

›Standing measurements at 1 minute

›SBP drop >=20 mmHg: diagnostic for OH

›DBP drop >=10 mmHg: diagnostic for OH

›Standing measurements at 3 minutes

›Delayed OH: drop occurring only at 3 minutes

›HR rise >=30 bpm without BP drop: consider POTS

›Symptomatic assessment during standing

›Lightheadedness, visual dimming during measurement

›Symptom correlation with BP drop

Cardiovascular exam

›Cardiac auscultation

›Aortic stenosis murmur

›Systolic ejection murmur at right upper sternal border

›Radiation to carotids

›HCM murmur

›Dynamic murmur increases with Valsalva and standing

›Decreases with squatting

›Irregular rhythm

›Atrial fibrillation

›Premature beats

›Peripheral perfusion

›Capillary refill time

›>2 seconds: low output state

›Peripheral pulse quality

04Differential Diagnosis/ddx51

Life-threatening mimics

›Cardiac etiologies

›Ventricular tachycardia

›ICD-10 I47.2

›Sudden onset, no prodrome, palpitations preceding

›High-degree atrioventricular block

›ICD-10 I44.2

›Bradycardia, slow recovery, ECG diagnostic

›Aortic stenosis

›ICD-10 I35.0

›Exertional syncope, harsh ejection murmur

›Hypertrophic cardiomyopathy

›ICD-10 I42.1

›Dynamic murmur, family history sudden death

›Pulmonary embolism

›ICD-10 I26.99

›Tachycardia, hypoxia, pleuritic pain, VTE risk factors

›Hemorrhagic etiologies

›GI hemorrhage

›Melena, hematemesis, or hematochezia

›Anemia, tachycardia, orthostatic vitals positive

›Ruptured aortic aneurysm

›Back or abdominal pain

›Pulsatile mass, shock physiology

Close mimics of orthostatic syncope

›Reflex syncope subtypes

›Vasovagal syncope

›ICD-10 R55

05Laboratory Tests/lt44

Core diagnostic labs

›Hematologic evaluation

›Complete blood count

›Hemoglobin: anemia as OH cause (CBC indicates etiology)

›Hemoglobin <80 g/L: significant anemia contributing to preload

›Leukocytosis: infectious trigger for dehydration

›Metabolic panel

›Serum electrolytes and renal function

›Sodium: hyponatremia, hypernatremia from dehydration

›Potassium: hypokalemia with diuretic use

›Creatinine and urea: prerenal azotemia from volume depletion

›Creatinine rise >26 mmol/l: AKI consideration

›Blood glucose (point-of-care)

›Hypoglycemia (<3.9 mmol/l): exclude as cause of LOC

›Hyperglycemia: osmotic diuresis contributing to dehydration

Cardiac biomarkers

›Troponin

›High-sensitivity troponin I or T

›Elevated: ACS or myocarditis as syncope trigger

›Serial at 0 and 3 hours if initial presentation

›99th percentile threshold varies by assay

›BNP or NT-proBNP

›BNP >100 pg/mL or NT-proBNP >300 pg/mL

›Cardiac dysfunction contributing to syncope

›Guides echocardiography decision

Additional targeted labs

›Thyroid function

›TSH

06Diagnostic Tests/dt95

Scoring Systems

›Canadian Syncope Risk Score (CSRS)

›Variables and scoring

›Heart disease predisposing to arrhythmia: +3

›Systolic BP <90 or >180 mmHg in ED: +2

›Abnormal QRS axis, duration, or repolarization: +2

›ED diagnosis: vasovagal trigger present: -2

›ED diagnosis: heart disease or primary arrhythmia: +2

›Troponin elevation above 99th percentile: +3

›Risk stratification thresholds

›Score <0: very low risk (~0.4%) — 30-day serious adverse event

›Score 0-3: low risk (~1%)

›Score 4-5: medium risk (~5%)

›Score >=6: high risk (~20%)

›Validated in prospective multicenter study

›AFP 2021 review endorses for ED risk stratification

›San Francisco Syncope Rule (SFSR)

›High-risk criteria

›Abnormal ECG

›History of congestive heart failure

›Shortness of breath

›Hematocrit <30%

›SBP <90 mmHg at triage

›Any criterion positive: high risk for serious outcome

›Sensitivity 98%, specificity 56% for serious outcome

›ROSE rule (Risk Stratification of Syncope in Emergency)

›High-risk features

›BNP >=300 pg/mL

›Bradycardia <=50 bpm in ED or on ECG

›Fecal occult blood positive or rectal bleeding

›Anemia (hemoglobin <90 g/L)

›Oxygen saturation <94%

›Q wave on ECG (not in V1)

›Sensitivity 87%, specificity 66% for serious adverse events

MRI

›Brain MRI

›Indications

›Suspected posterior circulation TIA or stroke

›New focal neurologic deficit

›Prolonged altered consciousness not explained by OH

›Protocol

›DWI sequence: acute ischemia

›FLAIR: subacute or chronic changes

›MRA brain and neck: vascular stenosis

›Role in syncope workup

›Not routinely indicated for isolated orthostatic syncope

›ACR Appropriateness Criteria: usually not appropriate for typical vasovagal or OH syncope

›Cardiac MRI

›Indications

›HCM characterization

›Arrhythmogenic cardiomyopathy (ARVC)

›Myocarditis with troponin elevation

›Not first-line in orthostatic syncope

›Reserved for structural cardiac suspicion after echo

CT

›CT head non-contrast

›Indications

›Head trauma from syncopal fall

›Anticoagulated patient after fall

›GCS <15 after event

›Focal neurologic signs

›Not indicated in uncomplicated OH syncope

›ACR Appropriateness Criteria: usually not appropriate without trauma or focal deficit

›Routine CT head in undifferentiated syncope: low yield <1% positive

›CT angiography of the chest

›Indications

›High PERC or Wells score for PE

›Persistent unexplained tachycardia and hypoxia

›D-dimer elevation in low-to-moderate risk patient

›Sensitivity and specificity for PE

›Sensitivity 83-100%, specificity 96% for subsegmental and larger PE

›CT abdomen and pelvis

›Indications

›GI hemorrhage suspected as OH trigger

›Suspected aortic aneurysm in elderly patient with abdominal pain

Ultrasound

›Point-of-care cardiac ultrasound (POCUS)

›Indications

›Unexplained hypotension after fluid resuscitation

›Suspected structural heart disease or HCM

›PE risk stratification (RV strain pattern)

›Key views

›Parasternal long axis: LV function, pericardial effusion

›Subxiphoid: effusion, RV dilation

›IVC: collapsibility for fluid responsiveness estimate

›Formal echocardiography

›Indications

›New murmur on exam

›Exertional syncope

›Abnormal ECG suggesting cardiomyopathy

›Elevated BNP or troponin

›Findings relevant to syncope

›LVEF: systolic dysfunction

›Aortic valve area: stenosis grading

›LVOTO gradient: HCM dynamic obstruction

›Carotid ultrasound

›Indications

›TIA evaluation: new focal deficit after syncope

›Not indicated for isolated OH syncope

07Disposition/dispo52

Discharge criteria

›Safe discharge parameters

›Clear orthostatic etiology

›Positive orthostatic vitals with consistent history

›Prodrome, positional trigger, rapid recovery on lying down

›No cardiac red flags present

›Normal ECG (no new BBB, QTc prolongation, ischemia, delta wave)

›No structural heart disease known or suspected

›No exertional syncope component

›Hemodynamically stable after treatment

›Asymptomatic at rest after rehydration or medication change

›Able to ambulate without presyncopal symptoms

›Reversible cause identified and addressed

›Medication discontinued or dose reduced

›Dehydration corrected with IV or oral fluids

›Safe home environment and reliable follow-up

›Fall risk mitigated (caregiver present or safe living situation)

›PCP follow-up within 1-2 weeks confirmed

Admission criteria

›Hospitalization indications

›Serious injury from syncopal fall

›Hip fracture (common in older adults)

›Head trauma requiring monitoring

›Intracranial hemorrhage

›Persistent symptomatic hypotension

›SBP <90 mmHg despite 1-2 L IV fluid

›Ongoing presyncopal symptoms standing

›Unexcluded cardiac etiology

08Treatment/t120

Immediate and acute measures

›Positional and physical interventions

›Supine positioning with leg elevation

›Head-of-bed flat or Trendelenburg

›Return venous blood to central circulation

›Effective within 30-60 seconds

›Counterpressure maneuvers (for prodrome prevention)

›Leg crossing with tensing of lower extremity muscles

›Squatting position during prodrome

›Abdominal compression with physical maneuver

›Class IIa recommendation per 2017 ACC/AHA/HRS guideline

Acute fluid replacement

›Intravenous hydration

›Normal saline 0.9% or Lactated Ringer's

›Initial bolus 500 mL over 15-30 minutes if hypotensive

›Titrate to symptom resolution and SBP >=100 mmHg

›Monitor for fluid overload in cardiac/renal patients

›Oral hydration if tolerated

›500 mL water bolus (rapid water drinking)

›BP rise within 5-15 minutes via water pressor reflex

›Class I recommendation per 2017 ACC/AHA/HRS guideline

Non-pharmacologic chronic management

›Lifestyle modifications

›Fluid intake

›Target 2-3 L total fluid per day

›Particularly important in morning before first standing

›Salt intake

›Increase dietary sodium to 6-10 g NaCl per day (2-3 g elemental sodium)

›Contraindicated in heart failure or severe uncontrolled hypertension

›Dietary modifications

›Small frequent meals rather than large carbohydrate-heavy meals

›Avoid alcohol (vasodilatory effect)

›Caffeine 100-250 mg before meals for postprandial OH

›Behavioral strategies

›Rise slowly from lying or sitting (sit at bedside 1-2 minutes before standing)

›Avoid prolonged standing >5-10 minutes

›Avoid hot environments, hot baths, and showers

›Physical measures

›Compression garments

›Thigh-high compression stockings (>=30-40 mmHg pressure)

›Abdominal binders for splanchnic pooling reduction

›Applied before rising in morning

›Elevation of head of bed at night

›30-45 degree head elevation (10-20 cm)

›Reduces overnight natriuresis

›Activates renin-angiotensin-aldosterone system during sleep

Pharmacologic therapy — first-line

›Midodrine (alpha-1 adrenergic agonist)

›Mechanism

›Peripheral vasoconstriction raising upright BP

›No CNS penetration

›Dosing

›Starting dose 2.5 mg PO 1-3 times daily

›Titrate to 5-10 mg PO 1-3 times daily

›Take with morning and midday doses only

›Timing

›Last dose at least 5 hours before bedtime

›Avoid supine use: causes supine hypertension

›Cautions

›Contraindicated in urinary retention, severe cardiac disease

›Monitor supine BP

›FDA approved for symptomatic OH

›Droxidopa (norepinephrine prodrug)

›Mechanism

›Converted to norepinephrine peripherally and centrally

›FDA approved specifically for neurogenic OH

›Dosing

›Starting dose 100 mg PO 3 times daily

›Titrate in 100 mg increments weekly

›Maximum 600 mg PO 3 times daily

›Last dose at least 3 hours before bedtime

›Preferred when supine hypertension coexists

›Less supine pressor effect than midodrine

›Cautions

›Monitor for supine hypertension

›Avoid in patients with severe supine HTN

Pharmacologic therapy — second-line

›Fludrocortisone (mineralocorticoid)

›Mechanism

›Volume expansion via sodium and water retention

›Sensitizes peripheral vasculature to catecholamines

›Dosing

›Starting dose 0.05 mg PO daily

›Titrate to 0.1-0.2 mg PO daily

›Monitoring

›Serum potassium at 1 week after initiation

›Monitor for hypokalemia

›Blood pressure monitoring for hypertension

›Contraindications

›Heart failure (absolute contraindication)

›Uncontrolled hypertension

›Significant hypernatremia

›Pyridostigmine (acetylcholinesterase inhibitor)

›Mechanism

›Enhances ganglionic neurotransmission

›Selectively raises upright BP without worsening supine HTN

›Dosing

›30-60 mg PO 1-3 times daily

›Preferred agent when coexisting supine hypertension

›Minimal effect on supine BP

›Side effects

›GI: nausea, diarrhea, cramping

›Urinary urgency

›Atomoxetine (norepinephrine reuptake inhibitor)

›Dosing

›10-18 mg PO 1-3 times daily

›Best when peripheral sympathetic neurons intact

›Multiple system atrophy (preganglionic nOH)

›Avoid in postganglionic denervation (pure autonomic failure)

Postprandial hypotension management

›Dietary approach

›Small frequent meals replacing large meals

›Reduces splanchnic pooling post-meal

›Caffeine 100-250 mg before meals

›Reduces postprandial BP drop by ~15 mmHg

›Acarbose 50-100 mg before meals

›Alpha-glucosidase inhibitor slows glucose absorption

›Reduces insulin-mediated vasodilation post-meal

Supine hypertension management (coexists in ~50% of nOH)

›Non-pharmacologic

›Head-of-bed elevation 30-45 degrees at night

›Reduces nocturnal pressure natriuresis

›Pharmacologic (bedtime only, short-acting agents)

›Clonidine 0.1-0.2 mg at bedtime

›Isradipine 5 mg at bedtime

›Atenolol 25-50 mg at bedtime

›All avoid during daytime to prevent further OH

09Special Populations/sp94

Pregnancy

›Physiologic changes affecting OH risk

›Supine hypotensive syndrome of pregnancy

›Uterine compression of IVC when supine

›Reduced venous return in third trimester

›Left lateral decubitus positioning recommended

›Normal OH-like physiology in first trimester

›Progesterone-mediated vasodilation

›Expanded intravascular volume but lower vascular resistance

›Postural changes amplified in pregnancy

›Rise slowly from lying to sitting to standing

›Avoid prolonged standing

›Evaluation in pregnancy

›Rule out pre-eclampsia

›BP elevation, proteinuria, edema

›ICD-10 O14.90

›Hemorrhagic causes

›Placenta previa or abruption

›Ruptured ectopic in first trimester

›Treatment approach in pregnancy

›Non-pharmacologic first-line

›Hydration, compression stockings, positional maneuvers

›Salt supplementation if not contraindicated

›Medications: safety data limited

›Midodrine: avoid (limited data, vasoconstriction concern)

›Fludrocortisone: use with caution, monitor BP and potassium

›Droxidopa: avoid (animal studies showed teratogenicity)

›Pyridostigmine: relatively safer; consult maternal-fetal medicine

Geriatric

›Epidemiology in older adults

›OH prevalence increases with age

›Prevalence 20-30% in community-dwelling adults >70 years

›Up to 50-65% in institutionalized elderly

›Leading cause of syncope in adults >65 years

›Accounts for majority of syncopal falls

›Associated with increased mortality

›JAMA Intern Med: OH independently associated with increased all-cause mortality

›Physiologic vulnerability

›Impaired baroreflex sensitivity with aging

›Delayed heart rate and vasomotor compensation

›Reduced thirst perception

›Chronic mild dehydration common

›Polypharmacy compounding effect

›Multiple BP-lowering agents

›Anticholinergic burden

›Reduced renal sodium conservation

›Nocturnal diuresis amplified

›Fall risk and injury prevention

›Hip fracture highest morbidity concern

›In-hospital mortality of hip fracture in elderly 5-10%

›1-year mortality after hip fracture 20-30%

›Head trauma risk

›Anticoagulated patients: low threshold for CT head

›PT/OT referral

›Gait and balance assessment

›Home safety evaluation

›Falls prevention program referral

›Treatment modifications in elderly

›Medication de-escalation first priority

›Deprescribing antihypertensives, diuretics, alpha-blockers

›ACC/AHA 2017: medication review essential (Class I)

›Fludrocortisone use cautiously

›Increased fluid retention risk

›Heart failure precipitation risk

›Midodrine dose start lower

›2.5 mg once daily initially

›Titrate slowly with BP monitoring

Pediatrics

›Orthostatic hypotension in children and adolescents

›Less common than vasovagal syncope in pediatric age group

›OH accounts for <10% of pediatric syncope presentations

›Dehydration as primary cause

›Adolescent athletes, particularly with heat exposure

›Poor fluid intake in active children

›POTS more common than classic OH in adolescents

›HR rise >=40 bpm on standing in age <19 (pediatric threshold)

›Predominantly female, ages 12-18

›Evaluation approach in children

›Orthostatic vitals with pediatric HR thresholds

›HR rise >=40 bpm in those <19 years for POTS diagnosis

›BP drop thresholds same as adults (>=20/10 mmHg)

›Tilt table testing

›Used to distinguish vasovagal, POTS, and OH

›Passive upright tilt 60-70 degrees for 10-45 minutes

›Treatment in pediatric patients

›Non-pharmacologic first-line

›Increased fluid intake: 2-3 L/day (age-appropriate)

›Salt supplementation: 2-3 g NaCl/day added to diet

›Physical reconditioning program

›Compression garments

›Pharmacologic only if non-pharmacologic fails

›Midodrine 2.5-5 mg PO 2-3 times daily

›Fludrocortisone 0.1 mg PO daily

›Evidence limited in pediatric population: off-label use

›Reassurance and education

›Most adolescent OH related to dehydration or deconditioning

›Prognosis good with lifestyle modification

10Background/b86

Epidemiology

›Prevalence and incidence

›OH accounts for approximately 9% of all syncope presentations

›Third most common syncope etiology after vasovagal and cardiac

›Overall OH prevalence in adults

›6% in community-dwelling adults aged 45-55 years

›20-30% in adults >70 years

›Up to 65% in institutionalized elderly

›Syncope overall affects 15-39% of general population during lifetime

›Annual incidence 1-2% in general population

›Outcomes and prognosis

›Prognosis generally favorable compared to cardiac syncope

›No direct cardiac mortality risk from OH mechanism itself

›Associated morbidity significant

›Falls and fall-related injuries: hip fracture, subdural hematoma

›Reduced quality of life, fear of falling, activity restriction

›Increased mortality in older adults with OH: likely marker of underlying disease

›Neurogenic OH carries worse prognosis

›Multiple system atrophy: median survival 9 years from diagnosis

›Parkinson disease autonomic failure: progressive course

Pathophysiology

›Normal orthostatic response

›On standing, 500-800 mL blood shifts to lower extremities and splanchnic bed

›Venous return decreases

›Cardiac output falls 20% transiently

›Compensatory baroreflex activation within 1-2 seconds

›Sympathetic nervous system increases HR and vascular tone

›Parasympathetic withdrawal

›Norepinephrine release from sympathetic nerve terminals

›Normal: SBP drop <10 mmHg, HR compensatory rise

›Stabilizes within 30 seconds

›OH mechanism — failure of compensation

›Hypovolemic OH

›Reduced intravascular volume (dehydration, hemorrhage, diuretics)

›Insufficient preload to maintain cardiac output on standing

›Neurogenic OH (nOH)

›Failure of sympathetic vasoconstriction

›Absent or blunted norepinephrine release on standing

›Preganglionic failure: MSA (central autonomic degeneration)

›Postganglionic failure: PD, PAF, DLB, diabetic autonomic neuropathy

›Medication-induced OH

›Volume depletion (diuretics), vasodilation (CCB, nitrates), sympatholysis (alpha-blockers, antidepressants)

›Supine hypertension paradox in nOH

›Absent sympathetic tone on standing but intact alpha-1 receptors respond to circulating NE when supine

›Present in ~50% of patients with nOH

›Cerebral autoregulation failure

›Chronic nOH causes shift in cerebral autoregulation curve

›Brain adapted to lower baseline perfusion pressure

›More vulnerable to acute drops

Therapeutic Considerations

›Treatment priority hierarchy

›Step 1: identify and remove offending medications

›Most important and effective intervention

›Medication-induced OH often fully reversible

›ACC/AHA/HRS Class I recommendation

›Step 2: correct underlying reversible cause

›Dehydration: IV or oral rehydration

›Anemia: transfusion or iron therapy

›Adrenal insufficiency: glucocorticoid replacement

›Step 3: non-pharmacologic measures

›Fluid and salt intake optimization

›Compression garments

›Behavioral modifications

›Step 4: pharmacotherapy for persistent OH

›Midodrine or droxidopa first-line

›Fludrocortisone second-line

›Combination therapy for refractory cases

›Distinguishing neurogenic from non-neurogenic OH

›Clinical clues to neurogenic cause

›Absent compensatory tachycardia on standing (HR rise <10 bpm)

›Coat hanger pain (highly specific for nOH)

›Features of autonomic failure: anhidrosis, urinary dysfunction, gastroparesis

›Parkinsonism or sensorimotor peripheral neuropathy

›Plasma NE testing (reference labs)

›Supine NE <100 pg/mL (<591 pmol/l): preganglionic (MSA pattern)

›Supine NE >100 pg/mL with blunted rise: postganglionic (PD/PAF pattern)

›Pharmacotherapy differs by subtype

›MSA (preganglionic): atomoxetine most effective

›PD/PAF (postganglionic): droxidopa FDA-approved, effective

›ICD-10 coding reference

›Primary OH codes

›G90.3: Multi-system degeneration of the autonomic nervous system

›I95.1: Orthostatic hypotension

›R55: Syncope and collapse (when etiology undetermined)

›Underlying cause codes

›G20: Parkinson disease

›G90.3: Multiple system atrophy

›E11.40: Diabetic autonomic neuropathy

›G62.9: Peripheral neuropathy (unspecified)

11Patient Discharge Instructions/pdi49

copy discharge instructions

›What happened today

›You fainted or nearly fainted due to a drop in blood pressure when you stood up

›This is called orthostatic hypotension or postural hypotension

›It is caused by blood pooling in your legs when you stand, reducing blood flow to your brain

›Steps to prevent fainting episodes

›Rise slowly from lying or sitting

›Sit at the edge of the bed or chair for 1-2 minutes before standing

›Stand up gradually, holding onto furniture for support

›Stay well hydrated

›Drink at least 2-3 litres of fluid per day

›Drink a large glass of water (500 mL) before getting up in the morning

›Increase your salt intake as directed by your doctor

›Add extra salt to food unless you have heart failure or are on a low-salt diet

›Salt tablets may be prescribed

›Avoid triggers

›Prolonged standing (>5-10 minutes)

›Hot showers, baths, or environments

›Large heavy meals (especially carbohydrate-heavy)

›Alcohol

›Counterpressure techniques if you feel dizzy

›Cross your legs and tighten the muscles

›Squat down to the ground if you feel a faint coming on

›Clench fists and tense arms

›Wear compression stockings if prescribed

›Put them on before getting out of bed in the morning

›Your medications

›Some of your medications may be making this worse

12References/r45

Guidelines and key sources

›2017 ACC/AHA/HRS Guideline for the Evaluation and Management of Patients With Syncope

›Shen WK, Sheldon RS, Benditt DG, et al.

›Journal of the American College of Cardiology, 2017

›Class I recommendation: 500 mL water bolus for OH management

›Class IIa recommendation: counterpressure maneuvers

›Class I: medication review and offending agent removal

›Management of Orthostatic Hypotension — JAMA Internal Medicine 2026

›Moloney D, Youssef A, Okamoto LE

›Comprehensive management algorithm for OH

›Fluid, salt, and pharmacologic treatment hierarchy

›Syncope: Evaluation and Differential Diagnosis — American Family Physician 2023

›Bayard M, Gerayli F, Holt J

›Midodrine dosing: 2.5-10 mg PO 1-3 times daily

›Fludrocortisone: 0.05-0.2 mg daily; avoid in HF

›Discharge and admission criteria

›Diagnosis and Treatment of Orthostatic Hypotension — Lancet Neurology 2022

›Wieling W, Kaufmann H, Claydon VE, et al.

›Coat hanger pain specificity for neurogenic OH

›Non-pharmacologic and pharmacologic management review

›Timing and triggers of OH episodes

›Orthostatic Hypotension in Adults With Hypertension — AHA Scientific Statement 2024

›Juraschek SP, Cortez MM, Flack JM, et al.

›Hypertension journal, 2024

›Management of coexisting hypertension and OH

›Pyridostigmine preferred when supine HTN present

›ACR Appropriateness Criteria — Syncope 2021

›Kligerman SJ, Bykowski J, Hurwitz Koweek LM, et al.

Evidence & Review