Approach to SYNCOPE

Dr yatendra singh

Syncope is defined as transient loss of consciousness due to reduced cerebral blood flow.

Syncope is associated with postural collapse and spontaneous recovery.

It may preceded by faintness or presyncope

This may include lightheadedness,dizziness without true vertigo, a feeling of warmth,diaphoresis, nausea and or visual blurring

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 (vertigo), hypoxemia, and hypoglycemia.

The differentiation of syncope from seizure is an important, sometimes difficult, diagnostic problem.

Syncope may be benign when it occurs as a result of normal cardiovascular reflex effects on heart rate and vascular tone or

Serious when due to life threatening arrythmias.

May be single episode or recurrent

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

Etiologies of Syncope

Neurocardiogenic / VasovagalMost Common

• Pain/Noxious Stimuli• Situational (micturation, cough,

defecation)• Carotid Sinus Hypersensitivity

(CSH)• Fear• Prolonged standing / heat

exposure

CardiovascularMost Dangerous

• Arrhythmia – Tachy or Brady• Valve Stenosis (outflow

obstruction)• HOCM (outflow obstruction)

Orthostatic Hypotension“ D A A D “

• Drugs: BP meds, Diuretics, TCAs• Autonomic Insufficiency

(Parkinsons, Shy-Dragger, DM, Adrenal Insufficiency)

• Alcohol• Dehydration

Neuro / Functional / Psychiatric - <5%

• Psuedosyncope• TIA or Vertibro-basilar Insufficiency

Pathophysiology

As blood pools in peripheral vessels and arterial blood pressure begins to fall, compensatory mechanisms are activated that attempt to maintain adequate cerebral blood flow.

These mechanisms include baroreceptors, which reflexely constrict peripheral blood vessels, increasing the return of venous blood to the heart, and the carotid and the aortic arch reflexes, which increases the heart rate.

These mechanisms work to increase the cardiac output and the maintenance of a close to normal blood pressure, all of which are seen during early presyncopal period

If the situation goes unmanaged these compensatory mechanisms fatigue, which is manifested through development of reflex bradycardia. ( cardioinhibitory component and vasodepressor component )

Slowing of the heart rate to less than 50 beats/min is common & leads to a significant drop of cardiac output which is precipitous fall in blood pressure to levels below the critical for maintenance of consciousness.

In such cases, cerebral ischemia results and the individual loses consciousness

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

Dizziness, lightheadedness, and fatigue, premonitory features of autonomic activation may be present

These include diaphoresis, pallor, palpitations, nausea, hyperventilation, and yawning.

Features of Neurally Mediated Syncope

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.

Reassurance Avoidance of provocative stimuli Plasma volume expansion with fluid and

salt are the cornerstones of the management of neurally mediated syncope.

Treatment: 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, 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.

Orthostatic Hypotension

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

Features

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

The first step is to remove reversible causes—usually vasoactive medications .

Nonpharmacologic interventions should be introduced.

Treatment: Orthostatic Hypotension

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.

Intravascular volume should be expanded by increasing dietary fluid and salt.

Nonpharmacologic interventions

If these nonpharmacologic measures fail, pharmacologic intervention with fludrocortisone acetate and vasoconstricting agents such as midodrine and pseudoephedrine should be introduced.

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.

Cardiac Syncope

Approach to the Patient

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.

Diagnostic Objectives

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 (EPS)

.

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 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

HISTORYEvents preceding

the syncopeProlonged standing

(vasovagal)Immediately upon

standing (orthostatic)With exertion (cardiac)Sudden without warning

or palpitations (cardiac)Aggressive dieting Heat exposureEmotional stress

Events during and after the episodeTrauma (implication

important)Chest pain (CAD, PE)Seizure (incontinence,

confusion, tongue laceration, postictal behavior)

Cerebrovascular syndrome (diplopia, dysarthia, hemiparesis)

Associated with n/v/sweating (vasovagal)

HISTORYAssociated symptoms

Chest pain, SOB, lightheadedness, incontinence

Past medical historyIdentifying risk factorsMorbidity and mortality

increases with organic causesParkinsons (orthostatic)Epilepsy (seizure)DM (cardiac, autonomic

dysfunction, glucose)Cardiac disease

MedicationsAntihypertensives,

diuretics (orthostatic)Antiarrthymics (cardiac

syncope)TCA, Amiodarone

(cardiac/prolonged QT)Family history

Sudden death (cardiac syncope/prolonged QT or Brugada)

PHYSICAL EXAMVital 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 rateTachy/brady, dysrhythmia

Respiratory rateTachypnea (pe, hypoxia,

anxiety)Bradypnea (cns,

toxicmetabolic)Blood pressure

High (cns, toxic/metabolic)Low (hypovolemia,

cardiogenic shock, sepsis)

PHYSICAL EXAMHEENT

Tenderness/deformity (trauma)

Papilledema (increased icp, head injury)

Breath (alcohol, dka)

NECKBruitsJVD (chf, mi, pe,

tampnade)

HEARTMurmur (valves,

dissection)Rub (pericarditis,

tamponade)LUNGS

Sounds may help distinguish chf, infection, pneumothorax

PHYSICAL EXAMABDOMEN

Pulsatile mass; AAATendernessOccult blood loss

PELVISBleeding, hypovolemiaTenderness (PID, ectopic,

torsion, sepsis)

SKINSigns of trauma,

hypoperfusionEXTREMITES

Paralysis (CNS)Pulses unequal

(dissection, embolus, steal)

PHYSICAL EXAMNEUROLOGIC

Mental status; toxic metabolic; organic disease; seizure; hypoxia.

Focal findings (hemorrhagic/ischemic stroke, trauma, tumor, or other primary neurologic disease

Cranial nervesCerebellar 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)

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.

Starting the “Workup”

Young adult, no comorbidity, normal ECG, absent orthostatics

VasomotorTry carotid massage

(+) carotid sinus sensitivity

(-) reflex or neurocardiogenic

MetabolicCheck chemistry. R/O

hypoglycemia, adrenal insufficiency

NeurologicCT head (tia, cva, sah)EEG (if suspect Sz)

CardiovascularIf Outflow obstruction,

check CT chest, Echo (PE, valvular, HOCM)

If venous return, check HCG, Echo (pregnancy, tamponade)

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 ECGKey Points

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

The ECG patient older, +comorbid signs/symptoms

Carotid Sinus Massage (CSM)Method1

Massage, 5-10 secondsDon’t occludeSupine and upright

posture (on tilt table)

Outcome3 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 neurologicalLess than 0.2%Usually transient

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.

Holter Monitoring

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

Loop Event Recorders

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

ECHOCARDIOGRAM

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

Structural Heart Disease

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)

EXERCISE STRESS TEST

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 testUnexplained

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

v/s SEIZURES

SYNCOPE

Upright posture Pallor present Unconscious-seconds Recovery-rapid Post-ictal confusion,

amnesia, headache-ABSENT

Injury-UNCOMMON Tongue biting-NEVER

SEIZURE

Any posture Pallor absent Unconscious-minutes/

hrs Recovery-slow Post-ictal confusion,

amnesia, headache-PRESENT

Injury-COMMON Tongue biting-

COMMON

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.

San Francisco Syncope Rule

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.

SUMMARY

Case 1

71y/o M presents after he passed out while walking up the stairs. He felt slightly lightheaded just prior to the event. Wife saw him fall but was able to quickly arouse him. He had no incontinence or tongue biting. Similar event occurred 2 weeks prior while he was doing yard-work for which he did not seek medical care. He has a long history of DM, and hypertension for which he takes Glipizide, Amlodipine, Lisinopril, and HCTZ. He does not drink. Vitals, orthostatics, and blood sugar are unremarkable. ECG shows left axis deviation and LVH. Exam shows 1+ bilateral edema and 4/6 ejection murmur radiating to the carotids.

What risk category is this patient and how would you proceed with workup?

Case 1

H/P, Orthostatics, ECG, Meds◦ ECG shows evidence of structural heart disease and

exam shows murmur. No orthostasis or suspicious history of vasovagal syncope. Patient has had multiple episodes.

Based on initial workup, patient is High Risko Needs Admission and Cardiac Work-up including

Echocardiogram and Stress Test Dx: Aortic Stenosis

Case 2

35y/o healthy M presents with an episode of syncope while standing. He did not experience any prodrome symptoms. This has never happened before. He has no medical history and uses no medications, drugs, or EtoH. Physical exam and ECG are normal. No orthostasis. Carotid massage is negative. Routine labs are unremarkable.

What risk category is this patient and how would you proceed with workup?

Case 2

H/P, Orthostatics, ECG, Meds - normal with no obvious cause of syncope

Patient is Low Risk and has had only a Single Episode of syncope No Further Work-up Indicated

What if the same patient presented with syncope while working out at the gym and physical exam showed a grade III systolic murmur that increased with Valsalva?o Patient is now High Risk given possible structural heart

disease and exertional syncope Admit to telemetry for cardiac work-up including

Echocardiogram to evaluate for Hypertrophic Cardiomyopathy.

Key Points

• Key Differential Dxo Vasovagal/Neurocardiogenic - most commono Cardiac – HIGH RISK PATIENTS, most dangerouso Orthostatic – “D A A D”o Other - Neurologic, Functional, Psych

• Work-up and Risk Stratificationo H/P, Orthostatics, Meds, ECG, +/- Carotid Massageo Risk Stratify

High Risk - Admit w/ cardiac work-up Low Risk - Outpatient workup based on frequency of episodes

• Brain Imaging ONLY if focal Neuro Deficits or Head trauma

THANK YOU