evaluation of syncope in adults
TRANSCRIPT
EVALUATION OF SYNCOPE IN ADULTS
Dr.Venkat Narayana Goutham.V
• Syncope(SING-kə-pee) is a transient, self-limited loss of consciousness with loss of postural tone due to acute global impairment of cerebral blood flow.
• The onset is rapid, duration brief, and recovery spontaneous and complete without medical or surgical intervention.
• Other causes of transient loss of consciousness need to be distinguished from syncope.
• These include seizures, vertebrobasilar ischemia, hypoxemia, and hypoglycemia
Syncope: Etiology
OrthostaticCardiac
Arrhythmia
StructuralCardio-
Pulmonary
1• VVS• CSS• Situational
CoughPost- Micturition
2• Drug-Induced• ANS FailurePrimarySecondary
3• Brady
SN Dysfunction
AV Block
• TachyVTSVT
• Long QT Syndrome
4 • Acute
Myocardial Ischemia
• Aortic Stenosis
• HCM• Pulmonary
Hypertension• Aortic
Dissection
Neurally-Mediated
Unexplained Causes = Approximately 1/3
Neurally Mediated (Reflex )Syncope--what happens?• Stress causes an
abnormal autonomic reflex
• Normal increased sympathetic tone replaced by increased vagal tone
• Variable contribution of vasodilation and bradycardia.
• Examples include syncope from:– Pain and/or fear– Carotid sinus
hypersensitivity– “situational” (cough,
micturition, defecation syncope)
Neurally Mediated Syncope
Features of Neurally Mediated Syncope
• dizziness, lightheadedness, and fatigue, premonitory features of autonomic activation may be present. These include diaphoresis, pallor, palpitations, nausea, hyperventilation, and yawning.
• During the event proximal and distal myoclonus (typically arrhythmic and multifocal) may occur, raising the possibility of epilepsy.
• The eyes typically remain open and usually deviate upward. Urinary but not fecal incontinence may occur.
Treatment: Neurally Mediated Syncope
• Reassurance• avoidance of provocative stimuli• plasma volume expansion with
fluid and salt are the cornerstones of the management of neurally mediated syncope.
• Isometric counterpressure maneuvers of the limbs (leg crossing or handgrip and arm tensing).
• Fludrocortisone, vasoconstricting agents, and beta-adrenoreceptor antagonists are widely used by experts to treat .
Orthostatic Hypotension
• Orthostatic hypotension, defined as a reduction in systolic blood pressure of at least 20 mmHg or diastolic blood pressure of at least 10 mmHg within 3 minutes of standing or head-up tilt on a tilt table.
Features
• It is a manifestation of sympathetic vasoconstrictor (autonomic) failure .
• light-headedness, dizziness, and presyncope (near-faintness)
• Visual blurring may occur, likely due to retinal or occipital lobe ischemia.
• Patients may report orthostatic dyspnea
• Neck pain—typically in the suboccipital, posterior cervical, and shoulder region (the "coat-hanger headache") most likely due to neck muscle ischemia, may be the only symptom.
• Symptoms may be exacerbated by exertion, prolonged standing, increased ambient temperature, or meals
Treatment: Orthostatic Hypotension
• The first step is to remove reversible causes—usually vasoactive medications .
• Nonpharmacologic interventions should be introduced.
Nonpharmacologic interventions• patient education regarding staged
moves from supine to upright• warnings about the hypotensive
effects of meal ingestion• instructions about the isometric
counterpressure maneuvers that increase intravascular pressure (see above).
• Intravascular volume should be expanded by increasing dietary fluid and salt.
• If these nonpharmacologic measures fail, pharmacologic intervention with fludrocortisone acetate and vasoconstricting agents such as midodrine and pseudoephedrine should be introduced.
Cardiac Syncope
• Cardiac (or cardiovascular) syncope is caused by arrhythmias and structural heart disease.
• Both cause the heart to be unable to sufficiently increase cardiac output to meet demand.
• Cardiac arrythymias especially in the elderly have high mortality.
Approach to the Patient
Diagnostic Objectives
• Distinguish true syncope from syncope mimics
• Determine presence of heart disease
• Establish the cause of syncope with sufficient certainty to:– Assess prognosis confidently– Initiate effective preventive
treatment.
• Generalized and partial seizures may be confused with syncope.
A Diagnostic Plan is Essential
• Initial Examination–Detailed patient history–Physical exam–ECG–Supine and upright blood pressure
• Monitoring–Holter–Event–Insertable Loop Recorder (ILR)
• Cardiac Imaging• Special Investigations
–Head-up tilt test–Hemodynamics –Electrophysiology study
.
Diagnostic Flow Diagram Initial Evaluation
Treatment
Syncope Not Syncope
Certain Diagnosis
Unexplained Syncope
Cardiac Likely
Cardiac Tests
Neurally-Mediated or Orthostatic Likely
Tests for Neurally-Mediated Syncope
Frequent or Severe Episodes
Tests for Neurally-Mediated Syncope
Single/Rare Episodes
No Further Evaluation
Confirm with Specific Test or
Specialist Consultation
Suspected Diagnosis
+ - + - + -
Treatment Treatment
Re-AppraisalRe-Appraisal
Treatment
HISTORY
• HISTORY alone identifies the cause up to 85% of the time
• POINTS– Previous episodes– Character of the events, witnesses– Events preceding the syncope– Events during and after the episode
HISTORY• Events preceding
the syncope– Prolonged standing
(vasovagal)– Immediately upon
standing (orthostatic)– With exertion (cardiac)– Sudden without
warning or palpitations (cardiac)
– Aggressive dieting– Heat exposure– Emotional stress
• Events during and after the episode– Trauma (implication
important)– Chest pain (CAD, PE)– Seizure (incontinence,
confusion, tongue laceration, postictal behavior)
– Cerebrovascular syndrome (diplopia, dysarthia, hemiparesis)
– Associated with n/v/sweating (vasovagal)
HISTORY• Associated
symptoms– Chest pain, SOB,
lightheadedness, incontinence
• Past medical history– Identifying risk factors– Morbidity and mortality
increases with organic causes
• Parkinsons (orthostatic)
• Epilepsy (seizure)• DM (cardiac,
autonomic dysfunction, glucose)
• Cardiac disease
• Medications– Antihypertensives,
diuretics (orthostatic)– Antiarrthymics (cardiac
syncope)– TCA, Amiodarone
(cardiac/prolonged QT)• Family history
– Sudden death (cardiac syncope/prolonged QT or Brugada)
PHYSICAL EXAM• Vital signs
– Orthostatics—most important
• Drop in BP and fixed HR ->dysautonomia
• Drop in BP and increase HR -> volume depletion/ vasodilatation
• Insignificant drop in BP and marked increase in HR -> POTS
– Temperature• Hypo/hyperthermia
(sepsis, toxic-metabolic, exposure)
– Heart rate• Tachy/brady,
dysrhythmia– Respiratory rate
• Tachypnea (pe, hypoxia, anxiety)
• Bradypnea (cns, toxicmetabolic)
– Blood pressure• High (cns,
toxic/metabolic)• Low (hypovolemia,
cardiogenic shock, sepsis)
PHYSICAL EXAM• HEENT
– Tenderness/deformity (trauma)
– Papilledema (increased icp, head injury)
– Breath (alcohol, dka)
• NECK– Bruits– JVD (chf, mi, pe,
tampnade)
• HEART– Murmur (valves,
dissection)– Rub
(pericarditis, tamponade)
• LUNGS– Sounds may
help distinguish chf, infection, pneumothorax
PHYSICAL EXAM• ABDOMEN
– Pulsatile mass; AAA– Tenderness– Occult blood loss
• PELVIS– Bleeding, hypovolemia– Tenderness (PID,
ectopic, torsion, sepsis)
• SKIN– Signs of trauma,
hypoperfusion• EXTREMITES
– Paralysis (CNS)– Pulses unequal
(dissection, embolus, steal)
PHYSICAL EXAM• NEUROLOGIC
– Mental status; toxic metabolic; organic disease; seizure; hypoxia.
– Focal findings (hemorrhagic/ischemic stroke, trauma, tumor, or other primary neurologic disease
– Cranial nerves– Cerebellar
testing
• EKG---Cornerstone of workup– Arrhythmia, long qt, WPW, conduction abn.
• Routine Blood work—limited value• Radiology---limited value except if
abnormal exam• Other tests—depending of history and
exam– Glucose --hemoglobin --troponin
--CK (syncope vs seizure)
Starting the “Workup”
• If young adult and No comorbid conditions or symptoms
Most likely VASOMOTOR or ORTHOSTATIC .
*Clinicians may forego the ECG in young, healthy patients with an obvious cause of syncope.
Young adult, no comorbidity, normal ECG, absent orthostatics• Vasomotor
– Try carotid massage• (+) carotid sinus
sensitivity• (-) reflex or
neurocardiogenic
• Metabolic– Check chemistry.
R/O hypoglycemia, adrenal insufficiency
• Neurologic– CT head (tia, cva, sah)– EEG (if suspect Sz)
• Cardiovascular– If Outflow obstruction,
check CT chest, Echo (PE, valvular, HOCM)
– If venous return, check HCG, Echo (pregnancy, tamponade)
The ECGKey Points• Guidelines recommend EKG in the
evaluation of all patients with syncope.• Exception: young healthy patients with
an obvious cause of syncope• Abnormal ECG in 90% of patient with
cardiac syncope• Only 6% of patients with reflex
mediated syncope have abnormal ECG.• Syncopal patient with negative cardiac
history and normal ECG—unlikely to have a cardiac cause
The ECG patient older, +comorbid signs/symptoms• If Abnormal ECG
– Ischemia/injury– Dysrhythmia
• Sinus brady, BBB, AV block, prolonged QT, WPW, HOCM, Brugada
• If Normal ECG– Consider holter or event recorder if
dysrhythmia suspected
Carotid Sinus Massage (CSM)• Method1
– Massage, 5-10 seconds– Don’t occlude– Supine and upright posture
(on tilt table)• Outcome
– 3 second asystole and/or 50 mmHg fall in systolic BP with reproduction of symptoms = Carotid Sinus Syndrome
• Absolute contraindications2
– Carotid bruit, known significant carotid arterial disease, previous CVA, MI last 3 months
• Complications – Primarily neurological– Less than 0.2%– Usually transient
Holter Monitoring• 24-48 hour monitor—limited value
because of intermittent nature of arrhythmias
• Event recorder—more helpful. Patient must be conscious in order to activate unit.
• Establishes diagnosis in only 2-3% of patients with syncope if ECG is normal.
• Indicated in patients at highest risk for arrhythmia ie, abnormal ecg, palpitations, cad history, syncope when supine or with exertion.
Loop Event Recorders
• Provides longer monitoring—weeks to months
• Can activate the monitor after symptoms occur, thereby freezing in its memory the readings from the previous 2-5 minutes and the subsequent 1 minute
• In patients with recurrent syncope, arrhythmias were found during symptoms in 8-20%.
• Limitations: compliance, use of device, transmission
ECHOCARDIOGRAM
• Access structural causes of cardiac syncope– AS, MS, HOCM, atrial myoxoma
• Unlikely to be helpful in the absence of known cardiac disease or an abnormal ekg.
• INDICATIONS– Abnormal ECG ---history of heart disease– Murmur ---exercise assoc.
syncope
Structural Heart Disease• Aortic Stenosis
– Most common structural lesion associated with syncope in the elderly
• Hypertrophic Obstructive Cardiomyopathy– Vasodilatation (drugs/hot bath) can
induce syncope• Obstruction to Right Ventricular
Outflow– PE, pulmonary stenosis, pulmonary
htn
EXERCISE STRESS TEST
• Syncope during exercise is more likely to be related to an arrhythmia
• Post-exertional syncope is usually neurally mediated.
• Echocardiogram should be done prior to EST to r/o structural abnormality.
• INDICATION– Syncope during or shortly after
exercise (exertional syncope)
TILT TABLE TEST
• Changes in position to reproduce symptoms of the syncopal event.
• Positive tilt table test– Induction of
bradycardia and hypotension
– Considered diagnostic for vasovagal syncope
Indications for Tilt table test• Unexplained recurrent syncope or syncope
associated with injury in absence of structural heart ds.
• Unexplained recurrent syncope or syncope associated with injury in setting of organic heart disease after exclusion of potential cardiac cause of syncope
• Identification of neurally mediated syncope could alter treatment
• Evaluation of recurrent unexplained falls.• Evaluation of near syncope or dizziness
Tilt Table Test
• Unmasks Vasovagal syncope susceptibility
• Reproduces symptoms
• Positive Tilt Test*Prophylaxis treatment—beta blockers or disopyramide as well as SSRIs
*Recurrent symptoms and bradycardia may require pacemaker
Syncope Evaluation Flow Chart
--CLUES
Symptoms DiagnosisOccurs after sudden unexpected pain, sound, smell, or sightProlonged StandingAthletes post exertion
Vasovagal attack
Occurs after micturition, defecation, cough or swallowing
Situational Syncope
Event occurs in association with severe throat or facial pain
Glossopharyngeal or trigeminal neuralgia
Occurs with head rotation or pressure on the carotid sinus-tumors, tight collars or shaving
Carotid Sinus Syncope
Episodes occur immediately on standing
Orthostatic hypotension
Headaches are associated with the event
Migraines
Medications taken before Drug induced syncopeEvent is associated with vertigo, dysarthria or diplopiaEvent is associated with arm exercize
TIA/Subclavian Steal Syndrome
Pulse/BP differences between armsAortic dissection/SSS
Syncope occurs without prodrome and patient has underlying structural heart dz.
Arrythmia
San Francisco Syncope Rule
• Risk Factors– C History of CHF– H Hematocrit less than 30– E Non-sinus rhythm or new changes in EKG– S Systolic BP less than 90– S Shortness of breath------------- is a simple rule for evaluating the
risk of adverse outcomes in patient who present with syncope.
SUMMARY
• Shotgun approach is Not helpful.• EKG should be considered in all
patients.• Tilt table test can diagnosis vasovagal
syncope.• Neurologic testing is low yield and often
overused.• Holter monitoring, Echo, EST, EP
considered in patients at high risk for cardiac syncope.
• Patients remain undiagnosed in 34% of cases.
THANK YOU