2. • Transient loss of consciousness associated with loss of postural
tone
• Ultimately, it is the lack of oxygen to the brainstem reticular-
activating system loss of consciousness &
postural tone.
• Most commonly, an inciting event causes a drop in cardiac
output.
• Cerebral perfusion is re-established by autonomic regulation as
well as the reclined posture, which results from the event.
• Accounts for 3% of ED visits
3. 1. Neurally mediated syncope:
→ Reflex response causing vasodilatation and bradycardia
with resulting cerebral hypoperfusion
→ Vasovagal (common faint):-
Often incited by pain or fear
Prodromal findings are usually present.
Typically lasts <20 sec
Tilt-table testing is the gold standard to diagnose.
→ Carotid sinus syncope:-
• Cough, sneeze
• GI stimulation (e.g., defecation)
• Micturition
ETIOLOGY
4.
5. 2.Orthostatic:
i. Positional changes cause abrupt drop in venous return to heart
ii. Volume depletion: Severe dehydration (e.g., vomiting, diarrhea,
diuretics)
iii. Hemorrhage
3.Autonomic failure:
i. Diabetic or amyloid neuropathy
ii. Parkinson disease
iii. Drugs (e.g., β-blockers) and alcohol
4. Cardiac arrhythmias:
i. Typically sudden and without prodromal symptoms
ii. Tachydysrhythmia or bradydysrhythmia
iii. Inherited syndromes (e.g., long QT syndrome, Brugada syndrome)
iv. Pacemaker/implantable cardioverter defibrillator malfunction
6.
7. 5. Structural cardiac or cardiopulmonary disease:
i. Valvular disease (especially aortic stenosis)
ii. Hypertrophic cardiomyopathy
iii. Acute myocardial infarction
iv. Aortic dissection
v. Pericardial tamponade
6.Pulmonary embolus
7.Neurologic:
i. Transient spike in intracranial pressure that exceeds cerebral
perfusion pressure
ii. Postsyncopal headache is almost universal
iii. May be presentation of a subarachnoid hemorrhage
8.Cerebrovascular steal syndromes
10. SYNCOPE IN PREGNANCY
• Pregnant patients frequently experience
presyncope or syncope from various causes. 5%
of patients experience syncope, 28% experience
presyncope throughout their pregnancy.
• Placenta acts as an AV malformation, causing
decreased SVR that potentiates orthostatic
symptoms.
• Fetus lying on IVC can lead to neurogenic and
hypovolemic syncope.
• Pregnant patients at higher risk of
DVT/pulmonary embolism (PE), UTI, seizures
(preeclampsia), valvular incompetencies. Must
exclude these diagnoses in ED evaluation.
• Elderly with highest incidence as well as
increased morbidity.
• >1/3 will have numerous potential causes.
11. SIGNS AND SYMPTOMS
History
⇒ Prodromal symptoms:
Lightheadedness
Diaphoresis
Dimming vision
Nausea
Weakness
The following findings suggest an underlying life threat: p
Sudden event without warning
Chest pain or palpitations
12. • 6 Ps of a syncope history:
1. Preprodrome activities
2. Prodrome symptoms—visual symptoms, nausea
3. Predisposing factors—age, chronic disease, family history of sudden
death
4. Precipitating factors—stress, postural symptoms
5. Passerby witness—what did they see?
6. Postictal phase, if any—suggests seizure
13. Physical Examination
• Evaluate for trauma
• Orthostatic vital signs
• Check for difference in BP in both arms suggesting aortic dissection
or subclavian steal syndrome.
• Careful cardiovascular exam, including murmurs, bruits, and
dysrhythmias
• Rectal exam to check for GI bleeding
• Urine pregnancy test in reproductive-age female
• Careful neurologic exam
14. • Pediatric Considerations
⇒ Warning signs of a potential serious underlying disease:
Syncope during exertion
Syncope to loud noise, fright, extreme stress
Syncope while supine
Family history of sudden death at young age (<30 yr)
20. Prolonged monitoring of ECG Dysrhythmia
Echocardiography Heart failure, cardiomyopathy,
valvular disease
Exercise & chemical stress ECG MI
Cardiac & coronary artery imaging MI
Electrophysiologic study Dysrhythmia
Carotid ultrasound Stroke, TIA
Head -up tilt table test Orthostatic hypotension
EEG Seizures
Tests performed as IP or OP evaluation
24. DIFFERENTIAL DIAGNOSIS
• Seizure → most commonly mistaken for syncope:
Key differentiating factor is postictal confusion.
Brief tonic movements and urinary incontinence may be seen
with syncope.
• Metabolic disorders (e.g., hypoxemia, hyperventilation,
hypoglycemia)
• Toxicologic
• Stroke
• Psychogenic syncope
• Malingering
• Breath-holding spells in children
25.
26.
27. TREATMENT
• PRE HOSPITAL
• Oxygen Cardiac monitoring IV access
• INITIAL STABILIZATION/THERAPY
• Advanced cardiac life support (ACLS)
interventions for unstable patients
Oxygen Cardiac monitoring IV access with
normal saline fluid bolus in suspected
hypovolemia
• Consider coma cocktail—dextrose,
thiamine, and naloxone for persistent
altered mental status
28. ED Management
• ACLS interventions for dysrhythmias
• Standard regimens for acute myocardial infarction
• Control BP for subarachnoid hemorrhage and aortic dissection
• Consider thrombolytics for submassive PE.
• MEDICATION
• Dextrose: D50W 1 amp (50 mL or 25 g) IV (peds: D25W 2–4 mL/kg
IV)
• Naloxone: 2 mg IV or IM (peds: 0.1 mg/kg)
• Thiamine: 100 mg IV or IM (peds: 50 mg)
29. DISPOSITION
• Admission Criteria
⇒ San Francisco Syncope Rule
patients at high risk for serious short-term outcomes (“CHESS”):
• History of CHF
• Hematocrit <30%
• Abnormal ECG
• Patient complaint of shortness of breath
• Systolic BP <90 Other recommendations:
⇒ Suspected cardiac syncope must be admitted to monitored
bed GI bleeds consider intensive care unit bed
• Admit elderly patients with syncope.
30.
31. • Discharge Criteria
⇒ Neurally mediated syncope or orthostatic syncope from volume
depletion may be evaluated on outpatient basis with close follow-up, if
patient is reliable and has a good social structure.
⇒ Driving restrictions until cleared
• Do not assume vasovagal cause in syncope associated with headache or
chest pain.