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