syncope 2
TRANSCRIPT
Syncope
Ed Da Veiga, M.D.
August 20, 2008
Learning Objectives
• Recognize the vast etiologies of syncope
• Understand the importance of uncovering underlying organic heart disease
• Learn diagnostic and management strategies for neurally mediated syncope
You know, medicine is not an exact science, but we are learning all the time. Why, just fifty years ago, they thought a disease like your daughter's was caused by demonic possession or witchcraft. But nowadays we know that Isabelle is suffering from an imbalance of bodily humors, perhaps caused by a toad or a small dwarf living in her stomach.
Theodoric, Barber of York
Case Presentation
• 38 year old male with hangover on flight for honeymoon to St. Lucia
• Stewardess asks for medical assistance as patient “felt funny” and then “passed out”
• What do you want to know?
Overview
• Syncope is a symptom, not a disease
• In all forms, consists of a sudden decrease or brief cessation of cerebral blood flow
• Accounts for 3.5% of ER visits and 1-6% of all hospital admissions per year
Definition
• Sudden and brief loss of consciousness associated with a loss of postural tone, from which recovery is spontaneous
Distinguishing Syncope
• Dizziness, presyncope, and vertigo– No LOC or loss of postural
tone
• “Drop attacks”– Lead to falls without loss of
consciousness
– Sometimes sign of vertebrobasilar TIA (15%)
• Features to distinguish syncope from seizure– Prodromal/
Premonitory symptoms
– Precipitating event
– Events that follow it
Precipitants/Prodromal Symptoms
• LOC precipitated by pain, exercise, micturition, defecation, or stressful event usually syncope
• Sweating, nausea = syncope
• Aura = Seizure
• Disorientation/ LOC > 5 minutes usually seizure rather than syncope
Important information
• WITNESSES?
• Initial Assessment (especially HISTORY) will often lead to a clear diagnosis and help efficiently direct further workup and/ or treatment
• H and P leads to identification of cause in 45% of patients
Differential Diagnoses
• Neurally Mediated Syncope (24%)
• Vasovagal
• Situational
• Carotid Sinus
• Orthostatic Hypotension (10%)
• Psychiatric Disorders (2%)
• Neurologic Dz (10%)• Cardiac Syncope
• Organic Heart Disease (4%)
• Arrhythmias (14%)
• UNKNOWN (34%)• 50-66% may be
neurally mediated based on tilt-table studies
Soteriades, E., et al. Incidence and Prognosis of Syncope. NEJM 2002: 347:881
Structural Heart Disease
• Presence of a structural heart disease (CAD, CHF, Valvular Heart Disease, CHD) is the most important risk factor for predicting the risk of death
• Have ↑ risk of death at one year
• Most arrhythmias are found in these patients
Soteriades, E. et al. Incidence and Prognosis of Syncope. NEJM 2002; 347:883
Risk Factors
• Predictors of arrhythmic syncope or cardiac death at one year
• CHF• Ventricular tachyarrhythmias• Abnormal ECG• Age >45 years
• Presence of 2 or more of these is associated with >10% incidence of syncope or cardiac death
Cardiac Differential
Cardiac Syncope: LOC often w/o prodrome• Indicates Outflow Obstruction• AS, HOCM, PAH, Pulmonic Stenosis, PE
• MI, USA, Coronary Artery Spasm, Aortic Dissection
• Arrhythmias• Prolonged QT (either Congenital or Drug Induced)• AV Block, Sinus Node Dysfunction• Ventricular tachycardia• Arrhythmogenic right ventricular dysplasia• Supraventricular tachycardia (Wolff-Parkinson-White)
Neurally Mediated Syncope
• Most Common Causes• Vasovagal, Situational, and Carotid Sinus
Syncope• Results from sudden reflex mediated
hypotension/ and or bradycardia• Triggered by various stretch/
mechanoreceptors (carotid sinus, bladder, esophagus, respiratory tract
Carotid Sinus Syncope and Autonomic Dysfunction
Freeman, M. Neurogenic Orthostatic Hypotension. NEJM 2008; 358: 616
Neurally Mediated Syncope Pathophysiology
• Peripheral Venous Pooling causes sudden in peripheral venous return
• Leads to cardiac “hypercontractile” state which activates stretch receptors
• Neural traffic to brain mimics severe hypertension and provokes paradoxical bradycardia and in PVR
TIMBER!!!
Orthostatic Hypotension
• Decline of >20mm Hg in SBP/ 10mm Hg in DBP from supine to standing
• Supine HTN common in these patients
• Elderly especially vulnerable• ↓ Baroreceptor sensitivity, ↓ Cerebral Blood Flow,
↑ renal sodium wasting, ↓thirst response with aging
• Peripheral sympathetic tone impairment• Diabetic neuropathy, antihypertensive medication
Neurologic Causes
• Syncope rare manifestation of cerebrovascular disease
• Subclavian steal syndrome,
• Basilar Artery Migraine (syncope and HA)
• Vertebrobasilar insufficiency “Drop Attacks”
Diagnostic Evaluation
• H and P! – 45% of time can identify cause• CBC, BMP• ECG- Low yield but can be important clues to
look for underlying heart disease• CT Head, EEG: low yield• Echocardiogram/ Stress Test: Helpful when
presence of underlying cardiac disease cannot be determined clinically
History
• Time of day• Activities preceding (recurrent/at rest, exercise
associated, on standing)
• Prodromes, associated symptoms• Duration of LOC• Injuries • Medications, ingestions• Cardiac History
Kapoor WN. NEJM. 2000. 343(25): 1856-1862
Family History
• Sudden unexplained death
• Deafness
• Arrhythmias
• Congenital heart disease
• Seizures
• Metabolic disorders
• Myocardial infarction at young age
Physical Exam
• Pulse, blood pressure – taken supine and standing after 3 minutes
• Murmurs, clicks of outflow tract obstruction
• Neurologic examination
• Carotid Massage (if no bruit)
Arrhythmia Testing
• Telemetry• Holter: 12-24 hours
• symptoms w/ arrhythmia (5%) v. symptoms without arrhythmia (17%)
• External Loop Recorders : can wear for weeks to months
• Implantable Loop Recorders: Monitor for 12-18 months
• Provided diagnosis in 55% of pts with unexplained syncope compared to conventional methods
• EP Studies: Helpful with structural heart disease
Tilt Table Test
• Used to evaluate autonomic nervous system
• Evaluates predisposition to neurally mediated syncope
• Specificity of negative test 90%
Indications for Tilt Table Testing
• Unexplained recurrent syncope• Single episode associated with injury or in
settings that pose a high risk of injury• If organic heart disease is present, than after
cardiac causes have been excluded• Evaluation of recurrent syncope in setting
of autonomic failure• Assessment of recurrent, unexplained falls
Indications for Hospital Admission
• History of CAD, CHF, Ventricular Arrhthmia
• Accompanying Chest Pain
• Abnormal ECG
• Moderate to severe orthostatic hypotension
• Age > 70 yrs
• Resulting Trauma
Management
Management of Neurally Mediated Syncope
Grubb BP. NEJM. 2005. 352(10): 1004-1010
Patient Instructions
• Preventing Syncope or Vasovagal Spells• Avoid EtOH, lack of sleep, warm environment• Maintain adequate hydration and food intake• Avoid drugs that lead to hypotension• Avoid activities that precipitate syncope
• Preventing LOC or Injury• Assume supine position upon onset of prodrome• Avoid driving or other activities that could lead to
injury
Bibliography
• Kapoor, WN Syncope. NEJM 2000; 343: 1856-62
• Freeman, R Neurogenic Orthostatic Hypotension NEJM 2008; 358: 615-624
• Soteriades, et al. Incidence and Diagnosis of Syncope. NEJM 2002; 347:878-885
• Grubb, B. Neurocardiogenic Syncope. NEJM 2005; 1004-1010
Thanks!