Syncope
- Brief loss of consciousness with the inability to maintain postural tone
- Spontaneously resolves without medical intervention
- Accounts for 1-2% of ED visits
- Accounts for 6% of hospital admissions
Presyncope
- Feeling of imminent fainting without LOC
- Same physiologic process as syncope
Clinical
- History:
- Details of preceding events – Witnesses?
- Prodromal symptoms
- Duration of LOC
- Symptoms occurring after return of consciousness
- Previous illnesses, alcohol, or drug use
- PMH
- Prior Hx of syncope
- Medications
Physical Exam:
- Cardio: Murmurs
- Neuro: Focal neuro deficits
- Rectal: r/o GI bleeding
- Orthostatic BP – lying, standing, sitting
Types of Syncope
Presentation | Causes | Diagnose | Treatment | |
Arrhythmia | sudden with no prodrome | arrhythmia | EKG 24 hr Holter monitor or event recorder | Arrhythmia specific |
Mechanical Cardiac | Excersional | Valve issue | Echo | Valve lesion – dependent |
Neurogenic | No prodrome, sudden, + focal neuronal deficit | Posterior circulation | Carotid U/S, CT angiogram | Vascular disease |
Orthostatic | Orthostatic | Volume decreased (4D’s” diarrhea, dehydration, diuresis, and hemorrhage); AMS = DM, Parkinson’s age | Systolic change of 20 Diastolic change of 10 HR change of 15 | Fluid resolves intravascular volume depletion |
Vasovagal | Visceral organ stimulation => cough, sit down to pee Carotid bodies => boxers hit under the jaw, tight ties Psychogenic => sight of blood | Situational, reproducible, and + prodrome | beta-blockers |
Orthostatic Hypotension
MOA:
When moving to an upright position –> gravity shifts blood to lower extremities –> Sympathetic nervous system increase output and decreases parasympathetic output –> HR increases + SVR increases –> Increase in CO and BP
If the autonomic compensatory response is insufficient –> decreased cerebal blood blood flow –> syncope
Path:
- Ten second disruption of blood flow to cerebral cortices or to the brainstem, OR
- Reduction in cerebral perfusion by 35-50%
Common Causes:
- Intravascular volume loss
- Poor vascular tone caused by alpha receptor disorders
- Medications
- Erectile dysfx drugs
- Anti-HTNs
- Beta Blockers
- Diuretics
- Anti-dysrhythmics
- Anti-psychotics
- Antidepressants
- Antiparkinsonism drugs
- Nitrates
- ETOH
- Cocaine
Neurological Syncope
- Types:
- Vasovagal
- MOA: Associated with inappropriate vasodilation + bradycardia –> results in decreased vagal or sympathetic tone
- Triggers: prolonged standing or emotional distress, painful stimuli
- Prodrome symptoms:
- Vasovagal
- Lightheadedness
- +/- N/V
- Pallor
- Diaphoresis
- Feelings of warmth
- Common Causes:
- Exposure to unexpected or unpleasant stimuli
- – Sight, sound, smell
- – Fear
- – Pain
- – Emotional distress
- – Instrumentation
- Reflex Mediated Syncope – Prolonged standing or kneeling
- Carotid Sinus Syndrome
- Situational
- Trigger: cough, micturition, defecation. cardioinhibitory, vasodepressor or mixed, urinating, swallowing, neuralgia
- Situational
DDX:
- Must be dx of exclusion
- Syncope or Seizure
Cardiac Related Syncope
- Aortic stenosis, Hypertrophic Cardiomyopathy, Anomalous coronary arteries
- Syncope with exertion or during exercise
Ventricular arrhythmias- prior history of CAD, MI, cardiomyopathy or decrease ejection fraction
Sick Sinus, bradyarrhythmia, AV block- sinus pauses, increase PR or increase QRS duration
Torsades de point (acquired QT prolongation)- hypokalemia, hypomagnesemia, medication causing increase QT interval
Congenital long QT syndrome- Family history of sudden death, increase QT interval, syncope with triggers (e.g., exercise, startle, sleeping)
Cardiopulmonary Syncope
- Types:
- Valvular stenosis
- CMPY
- Pulmonary HTN
- Congenital heart disease
- Myxoma
- Pericardial disease
- Aortic dissection
- Myocardial ischemia/infarction
- PE
Dysthymias Syncope
- Bradydysrhythmias
- – Short or long QT syndromes
- – Stokes-Adams attack
- – Sinus node disease
- – 2nd or 3rd-degree heart block
- – Pacemaker malfunction
Tachydysrhythmias- – VTach
- – Torsade de Pointes
- – SVT
- – Afib/Aflutter