01Approach to the Critical Patient/attcp69

Immediate priorities

›Airway and breathing

›Airway patency

›Jaw tone and secretion management

›Positioning to maintain airway

›Breathing adequacy

›SpO2 on room air

›Respiratory rate and effort

›If airway compromise, protect airway immediately

›Prolonged unresponsiveness is not vasovagal until proven otherwise

›RSI preparation if GCS remains low

›Circulation and perfusion

›Hemodynamic targets

›SBP >= 90 mmHg

›MAP >= 65 mmHg

›HR 50 to 100 bpm

›Persistent hypotension after supine positioning triggers expanded workup

›IV access

›IV fluid resuscitation

›Continuous cardiac monitoring

›Arrhythmia detection priority

›12-lead ECG within first 10 minutes (Class I recommendation)

Key decision points

›Cannot-miss diagnoses to exclude first

›Cardiac arrhythmia

›Sustained or non-sustained VT on monitor

›High-degree heart block

›Structural heart disease

02History/hx95

Presentation characteristics

›Syncope event description

›Prodrome presence and duration

›Diaphoresis, nausea, warmth, pallor, lightheadedness

›Tunnel vision or auditory dulling

›Typical prodrome strongly supports vasovagal etiology

›Duration of loss of consciousness

›VVS typically <30 seconds

›>60 seconds raises concern for seizure or cardiac cause

›Recovery characteristics

›Rapid return to baseline supports VVS

›Postictal confusion or prolonged disorientation suggests seizure

›Post-event fatigue common in VVS

›Trigger identification

›Classic vasovagal triggers

›Prolonged standing in warm environment

›Emotional distress, fear, or anxiety

›Pain, blood draw, medical procedure

›Fasting or dehydration

›Situational reflex syncope variants

›Cough, micturition, defecation, swallowing, laughing

›Position at onset

›VVS almost never occurs in supine position

›Supine syncope strongly suggests cardiac etiology

Alarm features

›Red flags suggesting non-vasovagal cause

›Syncope during or immediately after exertion

›Cardiac arrhythmia or structural heart disease concern

›Requires urgent cardiac evaluation

›Syncope without any prodrome

›Sudden LOC without warning

›Significantly raises concern for cardiac cause

›Associated symptoms

›Chest pain or dyspnea preceding event

›Palpitations before LOC

›Witnessed cyanosis during event

›Family history concerns

›Sudden cardiac death in relative <50 years

›Inherited arrhythmia syndromes: Brugada, HCM, long QT

›Demographic and contextual red flags

›Age >60 with first syncopal episode and no clear trigger

›Cardiac cause more common in older adults

›Prodrome often absent or attenuated in elderly

›SBP <90 mmHg at presentation

›Persistent bradycardia or new murmur on exam

Past medical and medication history

›Relevant medical history

›Cardiac history

›Ischemic heart disease, heart failure, prior arrhythmia

›Valvular disease, congenital heart disease

›Any cardiac history significantly raises cardiac syncope likelihood

›Prior syncope episodes

›Number, frequency, and similarity to current event

›Recurrent stereotyped episodes over years support VVS

›Neurologic history

›Known seizure disorder

›Prior stroke or TIA

›Autonomic disorders

›Diabetes, Parkinson disease

›Autonomic neuropathy

›Medications contributing to syncope

›Antihypertensives

›Alpha-blockers, vasodilators, diuretics

›Nitrates, calcium channel blockers, ACE inhibitors

›Neuropsychiatric agents

›Dopaminergic agents, antipsychotics, sedatives

›Tricyclic antidepressants

›QT-prolonging drugs

›Other contributors

›Opiates

›Alcohol

Review of systems

›Cardiovascular symptoms

›Chest pain

›Palpitations

›Dyspnea on exertion

›Neurologic symptoms

›Headache, focal weakness, speech changes

›Seizure-like activity: tonic-clonic movements, tongue biting

›GI and metabolic symptoms

›Hematemesis, melena, hematochezia

›Symptoms of hypoglycemia: tremor, diaphoresis, confusion

›OB and psychiatric history

›Pregnancy status in women of childbearing age

›Anxiety, panic attacks, hyperventilation

Collateral history

›Witness account

›Pallor and diaphoresis observed

›Supports vasovagal mechanism

›Duration of unresponsiveness

›Brief LOC with rapid recovery supports VVS

›Cyanosis during episode

›Suggests cardiac arrhythmia

›Convulsive movements

›Tonic-clonic activity >30 seconds suggests seizure

›Brief myoclonic jerks can occur in VVS and do not indicate seizure

›Occupation and lifestyle context

›High-risk occupations: driving, operating machinery, working at heights

›Impact on quality of life

›Alcohol use and hydration habits

03Physical Exam/exam67

Vital signs

›Hemodynamic assessment

›Blood pressure both arms

›Differential >20 mmHg suggests aortic dissection

›Hypotension SBP <90 mmHg is a red flag

›Heart rate and rhythm

›Persistent bradycardia: <50 bpm warrants investigation

›Irregular rhythm: atrial fibrillation or arrhythmia

›Temperature

›Fever raises concern for infectious cause

›Respiratory rate and oxygen saturation

›Tachypnea and hypoxemia: PE or cardiac etiology

›Orthostatic vitals

›Measurement protocol

›Supine 5 minutes, then 1 minute and 3 minutes upright

›SBP drop >=20 mmHg = orthostatic hypotension

›DBP drop >=10 mmHg = orthostatic hypotension

›HR response to standing

›Rise >=30 bpm without BP drop suggests POTS

›No compensatory tachycardia in cardioinhibitory VVS

Cardiac exam

›Heart auscultation

›Murmurs

›Systolic murmur increasing with Valsalva suggests HCM

›Harsh crescendo-decrescendo murmur suggests aortic stenosis

›Rate and rhythm irregularities

›Gallops suggesting heart failure

›Rubs suggesting pericarditis

04Differential Diagnosis/ddx73

Life-threatening causes

›Cardiac arrhythmias

›Ventricular tachycardia or fibrillation

›ICD-10 I47.2

›Sudden LOC without prodrome, structural heart disease risk

›High-degree AV block

›Mobitz II or complete heart block

›ICD-10 I44.2 or I44.3

›Supraventricular tachycardia with rapid rate

›Palpitations preceding LOC

›Sick sinus syndrome

›Sinus pause >3 seconds

›Older age group

›Long QT syndrome

›ICD-10 I45.81

›Drug-induced or congenital

›Brugada syndrome

›ICD-10 I49.8

›Coved ST elevation in V1-V3

›Structural heart disease

›Hypertrophic cardiomyopathy

›ICD-10 I42.1

›Exertional syncope, systolic murmur increasing with Valsalva

›Severe aortic stenosis

›ICD-10 I35.0

›Exertional syncope, harsh systolic murmur

›Cardiac tamponade

›ICD-10 I31.9

05Laboratory Tests/lt44

Point-of-care testing

›Immediate bedside tests

›Glucose

›Exclude hypoglycemia as syncopal cause

›Low threshold <3.5 mmol/l for IV dextrose administration

›Hyperglycemia also relevant as metabolic cause

›12-lead ECG

›Mandatory in all syncope presentations

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

›Normal ECG plus no cardiac history makes cardiac syncope unlikely (LR 0.20)

Core labs in undifferentiated syncope

›Blood tests when etiology unclear or red flags present

›Complete blood count

›Anemia suggesting hemorrhagic or chronic cause

›Leukocytosis suggesting infectious etiology

›Metabolic panel

›Electrolytes: hyponatremia, hypokalemia as arrhythmia triggers

›Renal function for medication dosing and dehydration assessment

›Calcium and magnesium: electrolyte disturbance and arrhythmia risk

›Troponin

›Obtain when chest pain, exertional syncope, or ECG changes present

›Not routinely required in classic low-risk VVS presentation

›Elevated troponin in PE or ACS

›BNP or NT-proBNP

›When heart failure suspected clinically

›Elevated suggests cardiac etiology

›D-dimer

›When PE probability is low to intermediate by Wells score

06Diagnostic Tests/dt99

Scoring Systems

›Canadian Syncope Risk Score (CSRS)

›Validated ED risk stratification tool

›Multicenter validation across Canadian EDs: Thiruganasambandamoorthy et al., JAMA Internal Medicine 2020

›30-day serious adverse outcome risk stratification

›Variables scored

›Predisposition to vasovagal symptoms (-1 point)

›Heart disease history (+1 point)

›Systolic BP on arrival <90 or >180 mmHg (+2 points)

›Elevated troponin level above normal threshold (+2 points)

›Abnormal QRS axis (+1 point)

›QRS duration >130 ms (+1 point)

›QTc prolonged >480 ms (+2 points)

›Emergency physician diagnosis of vasovagal: not cardiac or unknown (-2 points)

›Risk categories

›Very low risk (score <=-2): <1% 30-day serious outcome; zero deaths in validation

›Low risk (score -1 to 0): <1% 30-day serious outcome

›Medium risk (score 1 to 3): ~3% 30-day serious outcome

›High risk (score >=4): ~20% 30-day serious outcome

›FAINT score (alternative tool)

›Variables

›Family history of sudden death (+1)

›Absence of prodrome (+2)

›Illness feeling before syncope (-1)

›Neurologic symptoms (+1)

›Trauma above the clavicle (+1)

›FAINT >=1 suggests non-vasovagal cause

›San Francisco Syncope Rule

›Prediction rule for serious outcome at 7 days

›Abnormal ECG

›Shortness of breath

›Systolic BP <90 mmHg at triage

›Hematocrit <30%

›History of congestive heart failure

›Any criterion positive = higher risk

›Sensitivity 96% for serious outcomes in original derivation; lower in external validation

›ROSE rule (Risk stratification Of Syncope in the Emergency department)

›Variables

›BNP >=300 ng/L

›Bradycardia <50 bpm on ECG or telemetry

›Rectal examination with positive fecal occult blood

›Anemia Hb <90 g/L

›Chest pain associated with syncope

›ECG showing Q waves (non-LBBB)

›Saturation <94% on room air

›One or more criteria present = high risk

MRI

›Brain MRI in syncope

›Role is limited in typical vasovagal presentation

›Not routinely indicated for classic VVS

›Reserve for suspected neurologic etiology

›Indications

›New focal neurologic deficits suggesting stroke or TIA

›Suspected posterior circulation event: diplopia, ataxia, dysarthria

›Suspected subarachnoid hemorrhage when CT head negative

›Cardiac MRI role

›Cardiomyopathy characterization when structural disease suspected

›ARVC or infiltrative disease evaluation

›Not a first-line ED test

›Limitations

›Availability and time constraints in ED setting

›Not appropriate for hemodynamically unstable patients

›Contraindicated with non-compatible implants

CT

›CT head

›Not routinely indicated for syncope evaluation

›Syncope alone without head trauma or focal deficits does not require CT head

›ACEP Level B recommendation against routine CT head in syncope

›Indications for CT head

›Head trauma from fall during syncopal episode

›Focal neurologic deficits

›Thunderclap headache suggesting SAH

›GCS not returned to baseline

›CT pulmonary angiography

›Indicated when PE probability intermediate or high (Wells score)

›Tachycardia, hypoxemia, pleuritic pain, VTE risk factors

›Sensitivity ~96%, specificity ~98% for PE

›CT aorta

›Indicated when aortic dissection suspected

›Tearing pain, pulse differential, hemodynamic instability

Ultrasound

›Focused cardiac POCUS

›Immediate structural assessment

›Gross LV function estimate

›Pericardial effusion and tamponade screen

›Aortic root dilation screen

›Inferior vena cava

›Volume responsiveness adjunct

›IVC collapsibility with inspiration

›Integrate with clinical exam; limitations apply

›ACEP Level B recommendation for POCUS in undifferentiated syncope

›Abdominal POCUS

›Aortic diameter assessment

›AAA screen in older adults with unexplained syncope

›>3 cm diameter threshold for AAA

›Free fluid in peritoneum

›Hemorrhagic cause: ruptured AAA, ectopic pregnancy

›Tilt table test

›Not an ED test; specialist-directed

›Reproduced hypotension or bradycardia confirms vasovagal or orthostatic mechanism

›Indicated when initial evaluation does not clearly establish diagnosis

›Useful for patient education on prodrome recognition

›Sensitivity ~66%, specificity ~90% for vasovagal syncope

07Disposition/dispo51

Discharge criteria

›Low-risk features supporting discharge

›Classic VVS clinical features

›Identifiable trigger and typical prodrome

›Brief LOC with rapid return to baseline

›No exertional or supine onset

›Normal investigations

›Normal 12-lead ECG

›Normal vital signs including orthostatics

›Normal or baseline neurologic exam

›No high-risk historical features

›No cardiac history: IHD, HF, arrhythmia, structural disease

›No family history of sudden cardiac death <50 years

›CSRS very-low or low-risk category

›Score <=-2 to 0: <1% 30-day serious outcome rate

›Zero deaths or ventricular arrhythmias in validation cohort

Admission indications

›Clinical features requiring admission

›Syncope during exertion or while supine

›Cardiac arrhythmia or structural disease workup

›Inpatient monitoring and cardiology input

›No prodrome or sudden LOC

›Associated chest pain, dyspnea, or palpitations

›Abnormal ECG

›QTc >500 ms

›Brugada pattern

›Preexcitation (delta wave)

›New conduction disease

08Treatment/t109

Acute ED stabilization

›Immediate positioning

›Supine position with legs elevated

›Cerebral perfusion restoration

›Effective for acute vasovagal episode

›Avoid standing the patient immediately

›Recurrence risk during vagal recovery phase

›IV access and fluids

›IV access if hemodynamically unstable or dehydration suspected

›Normal saline 0.9% 500 mL bolus for dehydration

›Repeat bolus if orthostatic hypotension persists

›IV access not required for typical low-risk VVS

›Treat identified precipitants

›Pain management for pain-triggered VVS

›Antiemetics for nausea

›Ondansetron 4 mg IV or PO

›Metoclopramide 10 mg IV as alternative

First-line management (all patients)

›Patient education (Class I recommendation per ACC/AHA/HRS 2017)

›Explanation of diagnosis

›Benign prognosis and natural history

›Remissions are common over time

›Trigger avoidance

›Prolonged standing in warm environments

›Dehydration, fasting, alcohol

›Blood draws and medical procedures when avoidable

›Prodrome recognition and response

›Sit or lie down immediately at onset of warning symptoms

›Elevate legs if possible during prodrome

Non-pharmacologic interventions (recurrent VVS)

›Physical counter-pressure maneuvers (Class IIa recommendation)

›Leg crossing

›Activate lower extremity muscle pump

›Most effective with sufficient prodrome time

›Squatting

›Increases venous return rapidly

›Best performed at first symptom onset

›Isometric hand grip

›Squeeze ball or interlock fingers and pull

›Raises blood pressure through sympathetic activation

›Abdominal contraction

›Increases intraabdominal pressure and venous return

›Most effective in patients <60 years with sufficient prodrome duration

›Salt and fluid intake (Class IIb recommendation)

›Increased dietary sodium

›Expand plasma volume

›Contraindicated in hypertension, heart failure, CKD

›Liberal fluid intake 2 to 3 L per day

›Prevent volume contraction

›Orthostatic training (Class IIb)

›Tilt training: progressive upright posture tolerance

›Uncertain sustained benefit in RCTs

›May help selected patients with orthostatic trigger

Pharmacologic therapy for refractory recurrent VVS

›Midodrine (Class IIa recommendation)

›Mechanism: alpha-1 adrenergic agonist; increases venous tone

›43% reduction in recurrence in meta-analysis

›Best available pharmacologic evidence for VVS

›Dosing

›2.5 to 10 mg orally three times daily

›Administer during waking hours only; not at bedtime

›Titrate from 2.5 mg TID upward based on response

›Contraindications

›Hypertension

›Heart failure

›Urinary retention

›Supine hypertension risk: measure supine BP

›Fludrocortisone (Class IIb recommendation)

›Mechanism: mineralocorticoid; plasma volume expansion

›Monitor serum potassium for hypokalemia

›Best evidence in younger patients with low-normal BP

›Dosing

›0.1 to 0.2 mg orally daily

›Check K+ at 1 to 2 weeks after initiation

›Contraindications

›Heart failure

›Significant hypertension

›Hypokalemia at baseline

›Beta-blockers (Class IIb recommendation, limited evidence)

›Mechanism: reduce sympathetic surge during prodrome

›RCTs largely negative; ESC rates Class III (not indicated)

›Consider in patients >=42 years per ACC/AHA

›Metoprolol succinate

›25 to 100 mg orally daily

›Not first-line; use only if other options contraindicated or failed

›Contraindications

›Bradycardia at baseline

›Significant reactive airway disease

›SSRIs (Class IIb, limited evidence)

›Mechanism: serotonin modulation of autonomic reflex

›Weak evidence overall; benefit in network meta-analysis

›Consider when concomitant anxiety or depression present

›Fluoxetine

›10 to 20 mg orally daily

›Initiate low and titrate

›Paroxetine

›10 to 20 mg orally daily

›Monitor for QT effects

›Reduce or discontinue hypotensive medications (Class IIb)

›Antihypertensives contributing to syncope

›Review full medication list

›Discuss with prescribing clinician before stopping

›Nitrates and vasodilators especially implicated

Pacemaker therapy (highly selected patients)

›Dual-chamber pacemaker consideration

›Indications: highly selected patients

›Age >=40 years

›Frequent severe recurrent VVS

›Documented cardioinhibitory response (asystole) on tilt table or ILR

›Benefit for cardioinhibitory type

›Reduces asystole duration during syncopal episodes

›Does not prevent vasodepressor component

›Not indicated for mixed or vasodepressor-predominant VVS

›ACC/AHA 2017 Class IIb for tilt-induced asystole in selected patients

09Special Populations/sp87

Pregnancy

›Physiologic considerations

›Increased syncope risk in pregnancy

›Vasodilation and venodilation of pregnancy

›Inferior vena cava compression in supine position

›Aortocaval compression by gravid uterus after 20 weeks

›Supine hypotensive syndrome

›Turn patient to left lateral decubitus position

›Relieves uterine compression of IVC

›Vasovagal syncope is common in pregnancy

›Particularly first and early second trimester

›Priority exclusions

›Ectopic pregnancy

›Urine or serum beta-hCG mandatory

›Pelvic ultrasound for intrauterine pregnancy confirmation

›Placental abruption

›Abdominal pain and vaginal bleeding

›Obstetric emergency

›Pulmonary embolism risk elevated in pregnancy

›Tachycardia and hypoxemia require evaluation

›Medication safety

›Midodrine: limited safety data in pregnancy; avoid if possible

›Fludrocortisone: category C; use only if clearly indicated

›Beta-blockers: generally safer profile; consult obstetrics

›Monitoring

›Fetal monitoring when viable gestation with maternal hemodynamic instability

›Obstetric consultation for all third-trimester syncope

Geriatric

›Atypical presentation

›Prodrome often absent or attenuated

›Differentiation from cardiac syncope more difficult

›Lower threshold for cardiac monitoring and admission

›Delirium may be the presenting feature

›Rather than clear description of LOC

›Collateral history from witnesses essential

›Injury risk from falls is significantly higher

›Hip fracture, intracranial hemorrhage from head injury

›Fall-related injury assessment mandatory

›Polypharmacy and autonomic dysfunction

›Multiple medications contributing to syncope

›Diuretics, antihypertensives, nitrates, alpha-blockers

›Medication review is high-yield intervention

›Autonomic neuropathy prevalence

›Diabetes and Parkinson disease common

›Orthostatic hypotension more prevalent

›QT prolongation risk higher

›Multiple QT-prolonging medications

›Baseline ECG QTc assessment critical

›Disposition bias toward admission

›Frailty and reduced physiologic reserve

›Limited home support structures

›Autonomic and cardiac causes more common than in young patients

›CSRS validated across age groups but clinical judgment essential in frail elderly

›Canadian Syncope Risk Score in elderly

›Validated for adults presenting to ED

›High-risk features even more compelling for admission in frail older adults

Pediatrics

›Vasovagal syncope is the predominant cause in children

›Accounts for >60% of pediatric syncope presentations

›Benign natural history; majority resolve spontaneously

›Reassurance and lifestyle measures are primary treatment

›Key pediatric exclusions

›Long QT syndrome

›Exercise-triggered or sudden syncope

›Family history of sudden death or drowning in young family member

›QTc >460 ms on ECG in children

›Wolff-Parkinson-White syndrome

›Delta wave and short PR on ECG

›HCM in adolescent athletes

›Exertional syncope with murmur

›Screen with ECG and echocardiography

›Myocarditis

›Viral prodrome, chest pain, elevated troponin

›Evaluation approach

›History and ECG sufficient for typical low-risk presentation

›Tilt table testing rarely needed in children

›Echocardiography if structural disease suspected

›Holter or event monitor if palpitations or exertional trigger

›Treatment in pediatrics

›Education and trigger avoidance: first-line

›Hydration counseling for children and parents

›Salt intake increase: 2 to 3 g extra sodium per day

›Counter-pressure maneuvers: adapt for child's ability

›Midodrine weight-based: 0.1 mg/kg per dose up to 2.5 mg TID

›Adolescent dosing: adult dosing approach

›Avoid beta-blockers in children: RCTs showed no benefit

›Pediatric athletic participation

›Structural and primary electrical disease excluded before return to sport

›VVS with classic features does not require activity restriction

›Cardiology input for any exertional or atypical syncope in athletes

10Background/b73

Epidemiology

›Prevalence and incidence

›Most common cause of syncope across all age groups

›Approximately two-thirds of syncope diagnoses are vasovagal

›Lifetime prevalence of at least one vasovagal episode: up to 40%

›Incidence peaks in two age groups

›Adolescents and young adults: 15 to 30 years peak

›Older adults: >70 years second peak with overlap of multiple causes

›Sex distribution

›Slightly more common in females

›Blood-injection-injury phobia subtype more common in women

›Healthcare burden

›Syncope accounts for 1 to 3% of all ED visits

›Vasovagal syncope accounts for majority of these

›Annual healthcare cost burden significant due to diagnostic workup

›Hospitalization rates range 12 to 86% depending on institution; many admissions potentially avoidable

›Prognosis

›Prognosis is benign with excellent long-term survival

›No increased mortality compared to general population

›Recurrence is common: 30 to 50% recur within 2 years without intervention

›Spontaneous remission occurs in approximately 50% over 4 years

›Quality of life impairment significant in recurrent severe VVS

Pathophysiology

›Central mechanism

›Bezold-Jarisch reflex

›Vigorous ventricular contraction on near-empty ventricle

›Activation of C-fiber mechanoreceptors in left ventricle

›Paradoxical withdrawal of sympathetic tone and vagal activation

›Result

›Inappropriate vasodilation: vasodepressor component

›Bradycardia or asystole: cardioinhibitory component

›Cerebral hypoperfusion causing LOC

›Triggering pathways

›Orthostatic stress

›Venous pooling in lower extremities on standing

›Reduced venous return and cardiac preload

›Emotional and pain triggers

›Central cortical and hypothalamic activation

›Direct vagal efferent stimulation

›Situational reflex pathways

›Cough: intrathoracic pressure mechanism

›Micturition: bladder emptying with Valsalva release

›Subtypes by dominant mechanism

›Vasodepressor (pure): >50% of cases

›BP fall without significant bradycardia

›Cardioinhibitory: less common

›Bradycardia or asystole dominant

›Responds best to pacemaker in selected patients >=40 years

›Mixed: both components present

›Most common tilt table finding

Therapeutic Considerations

›Why non-pharmacologic therapy is first-line

›VVS is largely a benign condition

›Pharmacologic side effects must be justified against benign prognosis

›Education and lifestyle modification have best evidence:risk ratio

›Recurrence is self-limiting in many patients

›Spontaneous remission supports conservative initial approach

›Pharmacologic evidence hierarchy

›Midodrine has strongest pharmacologic evidence

›Class IIa recommendation per ACC/AHA/HRS 2017

›43% recurrence reduction in network meta-analysis (Heart Rhythm 2023)

›Fludrocortisone has moderate evidence (Class IIb)

›Beta-blockers largely ineffective per RCT data; ESC Class III

›SSRIs have weak evidence; benefit mainly when anxiety comorbid

›Pacemaker rationale

›Only effective for cardioinhibitory subtype

›Prevents asystole but not vasodepressor component

›Patient selection critical: age >=40, documented asystole

›Implantable loop recorder (ILR) role

›Diagnoses cardioinhibitory subtype during spontaneous events

›Guides pacemaker eligibility decision

›Tilt table testing in management

›Documents subtype for treatment planning

›Provides patient education on prodrome recognition

›Guides decision for counter-pressure maneuver training

›ACC/AHA Class IIa for unexplained recurrent syncope evaluation

11Patient Discharge Instructions/pdi49

copy discharge instructions

›What happened to you

›You had a vasovagal faint

›Your blood pressure briefly dropped, reducing blood flow to your brain

›This caused you to lose consciousness temporarily

›This is the most common type of fainting and is not dangerous

›It does not mean you have a heart problem

›Your heart and brain are normal

›What triggers this type of fainting

›Common triggers to recognize and avoid

›Standing for a long time, especially in a warm or crowded place

›Dehydration: not drinking enough fluids

›Skipping meals or fasting

›Seeing blood, needles, or medical procedures

›Pain, emotional stress, or fear

›Alcohol

›What to do if you feel a faint coming on

›Warning signs: you may feel sweaty, nauseous, warm, lightheaded, or have tunnel vision

›Sit or lie down immediately

›Raise your legs if you can

›Tense your leg muscles or cross your legs to push blood back up

›Stay down until the feeling passes completely

›How to reduce future episodes

›Hydration

›Drink 2 to 3 litres of fluid per day

›Increase slightly with exercise or heat

›Salt intake

›Add extra salt to meals if your blood pressure is normal and no heart or kidney disease

12References/r38

Guidelines and key sources

›ACC/AHA/HRS Syncope Guidelines

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

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

›Journal of the American College of Cardiology. 2017

›Primary guideline for ED evaluation and management of syncope

›JAMA Rational Clinical Examination

›Albassam OT, Redelmeier RJ, Shadowitz S, et al.

›Did This Patient Have Cardiac Syncope? The Rational Clinical Examination Systematic Review

›JAMA. 2019

›Clinical features distinguishing cardiac from vasovagal syncope; LR data

›American Family Physician Review

›Bayard M, Gerayli F, Holt J

›Syncope: Evaluation and Differential Diagnosis

›American Family Physician. 2023

›Practical ED evaluation framework and risk stratification

Validation studies and pharmacologic evidence

›Canadian Syncope Risk Score Validation

›Thiruganasambandamoorthy V, Sivilotti MLA, Le Sage N, et al.

›Multicenter Emergency Department Validation of the Canadian Syncope Risk Score

›JAMA Internal Medicine. 2020

›Validated risk tool for 30-day serious outcome prediction

›Meisenheimer ES, Rogers TS, Saguil A

›Canadian Syncope Risk Score: A Validated Risk Stratification Tool

›American Family Physician. 2021

›Pharmacologic Prevention Meta-Analysis

›Behnoush AH, Yazdani K, Khalaji A, et al.

›Pharmacologic Prevention of Recurrent Vasovagal Syncope: A Systematic Review and Network Meta-Analysis of RCTs

Evidence & Review