Syncope and Loss of Consciousness

Last Updated: 1/9/2023

# Syncope
# Loss of Consciousness (LOC)

-- Chart Check: prior admissions, EKG, Echo, h/o heart disease, seizures, clotting
-- Admission Criteria: yes if red flags, or EKG is newly non-sinus, dyspnea, anemia, hypotensive, h/o heart failure
-- Thorough HPI Intake: Are there any red flags for cardiac syncope or other etiologies
-- Can't Miss: PE, Arrythmia, Aortic Stnosis, Seizure, Stroke/TIA, Hemorrhage
-- Admission Orders: for all - CBC, BMP, trop, NT-proBNP, EKG, telemetry
-- Other Workup: Get orthostatics, if concern for other etiology consider echo, CTPE, CT Head
-- Initial Treatment to Consider: Give fluid

-- Witnessed: *** manner of collapse, duration down, rythmic movements
-- Inciting Events: *** after prolonged standing, upon staning, stressors, pain, PO intake, hot weather
-- Prodrome: *** dizziness, nausea, abdominal pain, warmth/flushing
-- Associated Symptoms: *** tongue laceration (side vs front), loss or urine or stool, palpitations, chest pain, SOB
-- Recovery Time: *** confusion, nausea/vom
-- Head Strike: *** lucid interval
-- Intoxication: *** EtOH, benzos, opioids
-- Meds: *** opioids, benzos, TCAs, hypnotics, anti-cholingergics, blood thinners
-- History and Comorbidities: *** seizure, diabetes, CAD, CHF, valvular disease, arrythmia, PE risk factors (malignancy, asymmetric leg swelling, etc)
-- Red Flags: *** palpitations, chest pain, SOB, exertional, supine, no prodrome

-- History
: *** head trauma, poor PO intake, GI losses, FHx SCD, co-morbidities, contributing meds
-- Clinical: ***  prodrome/aura - dizzy, nausea, warmth, diaphoresis - exertional, tongue biting, incontinence, post-ictal
-- Exam: *** orthostasis, tachycardia, general appearance, volume assessment, rythm, murmur, S3, crackles, LE edema, focal neuro deficits
-- Data: *** Hgb, Trop, NT-proBNP, UDS, EKG, Echo
-- Etiology/DDx: *** reflex (vasovagal, situational), orthostasis (autonomic failure, meds), volume (decreased PO, GI losses, hemorrhage), cardiac (AS, PE, arrhythmia, AV block), neurologic (seizure, stroke/TIA), intoxication (EtOH, benzo, opioids), mechanical fall, hypoglycemia, hypoxia, psychiatric

The patient's HPI is notable for ***. Exam showed ***. Labwork and data were notable for ***. Taken together, the patient's presentation is most concerning for ***, with a differential including ***.

-- f/u orthostatics (change of >20/10)
-- Labs: *** f/u troponin, NT-proBNP; consider UDS; if orthostatic - A1c, SPEP, RPR, B12
-- Imaging: *** EKG, telemetry and Echo or stress test (if concern for cardiac etiology), EEG (if concern for seizure), CT Head (if head strike, blood thinner use, focal deficit), CTPE (if workup unremarkable and first syncopal event)
-- if c/f arrythmia - consider Holter Monitor/Zio Patch vs Event recorder vs Loop Recorder
-- if c/f autonomic failure - tilt table in outpatient setting
-- IVF PRN - now s/p ***
-- if Reflex - avoid provocative stimuli, trial counterpressure maneuvers (leg cross, hand grip, valsalva)
-- if Orthostasis - treat underlying etiology, replete volume, slow rising, waist-high compression stockings, abdominal binders, increased salt intake, d/c contributing meds;  midodrine 5-20mg TID during waking hours and upright, fludrocort 0.1-0.2 qD, droxidopa
-- if Cardiac - address underyling etiology

If You Remember Nothing Else

While common, syncope is only one of the major causes of loss of consciousness (LOC). It must be transient, self-limited, and with a complete recovery.

A good HPI is key, and red flags suggesting a cardiac etiology include palpitations, chest pain, shortness of breath, exertional syncope, no prodrome, and syncope while supine. Everyone should get EKG, trop, BNP, and telemetry with more advanced workup saved for those with concerning presentation or co-morbidities. If you have confidently ruled out reflex and orthostatic syncope, you should have a high suspicion for a cardiac etiology.

Orthostasis is defined by a drop in >20 SBP or >10 DBP upon positional change; methods differ, but a good rule of thumb is to check after 3 minutes of standing from a lying position, and you should clarify what was actually done at the bedside. Most cases can be treated with supportive care and lifestyle changes, but some patients with orthostasis may require treatment, usually with midodrine or fludrocort.

Clinical Pearls

  • Syncope is defined as transient (short duration), self-limited LOC with complete spontaneous recovery, associated with loss of postural tone, and due to cerebral hypoperfusion (aka hypotension) - it should be abrupt and brief
  • A diagnosis of syncope excludes hypoglycemia, hypoxia, intoxication and other causes such as neurological
  • Concerning features of syncope warranting workup and admission (to investigate cardiac etiology) include: palpitations, no prodrome, exertional, abnormal EKG, LOC when supine, underlying heart disease
  • The most common causes of syncope are reflex (60%) which includes vasovagal and situational; then orthostatic (15%) which can be caused by meds and autonomic failure; then cardiac (15%) which s the most concerning etiology
  • Vasovagal - stimulation of vagal nerve leads to bradycardia and vasodilatation which both drop CO and BP - has to be triggered
  • Likelihood Ratios for Vasovagal Syncope - Prolonged standing (+9), abdominal discomfort (+8), and happening during injection/cannulation (+7); check out this great review of likelihood ratios
  • Orthostasis is defined as a drop in systolic 20mmHg or diastolic 10mmHg within 3 minutes of standing (from lying)
  • Orthostasis can be caused by autonomic failure - differential include Parkinsons, Lewy Body, Shy-Drager, amyloid, B12 deficiency, and diabetes
  • Common culprit medications that can cause orthostasis include diuretics, vasodilators, beta blockers, and alpha blockers
  • If there is a large increase in HR with orthostatic symptoms, that is POTS (Postural Orthostatic Tachycardia Syndrome), but HR response is not part of the typical definition of orthostasis (though if HR >30 increase, it's likely related to symptoms)
  • To check orthostatics, get BP lying and then immediately after standing and then 3 minutes after standing - goal to mimic when people are at most risk for falling at home when they get up from bed; do not assume that nursing will know how you'd like this to be performed - be specific!
  • Historically, a HR jump <15 bpm upon standing when checking for orthosatsis indicates a neurogenic etiology, but that was based on expert opinion. A newer proposed metric of [change HR / change SBP] < 0.5 was suggested to be diagnostic of neurogenic etiology (Ann Neurol, 2018)
  • If it’s orthostatic, that's good because it's usually not life-threatening, but still need to figure out why!
  • If it’s not reflex or orthostatic syncope, then it is cardiac!
  • You may not catch an arrythmia while inpatient and will recommend a patient have ambulatory monitoring. Options for outpatient monitoring include Holter Monitors and ZioPatch which continuously record for 24-48 hours. Event recorders only record when patient pushes button when they experience symptoms like palpitations. Loop recorders record over long periods of time, but deletes most of the data unless patient has syncopal event in which case patient pushes button upon awakening and the device keeps the data leading up to that event for further analysis. YouTube Video exlaining different ambulatory hear monitors
  • Cardiac syncope in a young person - look on EKG for WPW (delta wave), LVH, Brugada (coved ST elevation), long-QT, ARVC (Epsilon wave)
  • You can have loss of urine in both syncope and seizure, despite classic teaching that this can help distinguish them
  • Similarly, classic teaching suggests tongue biting in seizure is on the sides vs the front in syncope, however this is not validated
  • Romeo Score - includes (CHF, CAD, abnormal EKG, hsTNT >14, NT-proBNP >125) - if all negative, can forgo getting a TTE inpatient - score of 0 led to 0.8% risk of major finding as cause of syncope; If no criterion is met, the likelihood of clinically significant echocardiographic findings to explain syncope is very low; yet about 7% of inpatients get echo which leads to high costs (J Hosp Med, 2018)
  • 3% of patients who get echos inpatient are found to have structural lesions, with <1% having new aortic stenosis
  • If you have do have mod-severe aortic stenosis, you will almost certainly have a murmur - you don’t need to get an echo to go looking for it, just listen!
  • Can generally avoid carotid dopplers if no focal deficits - very rare for a stroke to lead to global hypoperfusion that would lead to syncope; the notable exception is a TIA in the vertebrobasilar distribution

Trials and Literature

  • 2017 Guidelines for Evaluation and Management of Patients with Syncope (J Am Coll Cardiol, 2017)
  • PE was identified in 17.3% of hospitalized patients with first episode of syncope - though note that this included incidental findings (small PE's that likely were not the etiology of the syncope), as well as PE's that were likely chronic; thus the actual incidence of PE causing syncope is probably much lower, but should stay on the differential in patients who fit the illness script (NEJM, 2016)
  • Rational Clinical Exam - Cardiac Syncope (JAMA, 2019)
  • Romeo Score ; Original Article (J Hosp Med, 2018)

Other Resources