Syncope

AN APPROACH TO A PATIENT WITH

SYNCOPE

BY:Dr. Tikal Kansara

R2 Medicine D Unit

What is Syncope?

• Transient, self-limited loss of consciousnesswith an inability to maintain postural tone that is followed by spontaneous recovery.

with global cerebral hypoperfusion

Aka swoon, blackout, collapse, faint

• Pre-Syncope/ Almost fainting:– A state consisting of lightheadedness, muscular

weakness, blurred vision, and feeling faint (as opposed to a syncope, which is actually fainting).

•FaintnessSensation of impending loss of consciousness

•GiddinessHaving a reeling, light headed sensationA feeling of unease and unsteadiness

• Vertigo– A sensation of rotation of one’s self (subjective

vertigo) or one’s surroundings (objective vertigo) in any plane.

• Dizziness– Vertigo– Syncope– Nonsyncope Nonvertigo• Patients feel that they cannot keep their balance• May become worse on movement

Why is it important?

• Syncope can be an isolated benign, stand alone incident or it can be a trigger of some serious life threatening condition; most likely CARDIAC.

• Hence, it is important to be vigilante to scrutinize this symptom

MECHANISM OF SYNCOPE

• Syncope is the result of global cerebral hypoperfusion.

• Brain parenchyma cannot store high energy phosphate bonds like other cells of the body hence depends on the constant supply of glucose for its survival.

• Typically cessation of blood supply for 3 to 5 seconds results in syncope.

Reproduced From: European Heart Journal (2009) 30, 2631–2671

BIO DATA

• Age:– Two peaks: • With median of 15 years – VVS (Vasovagal Syncope) is

more common• With old age patients – Cardiac & OH is more common

• Sex: More common in females• Occupation: – Common in painters, formal clothing (tight collar

and tie)

HISTORY

• Hx and PE are perhaps the two most important aspects in diagnosis of Syncope.

• These (Hx & PE) with 12 lead ECG is the only Level A recommendation for diagnosis of Syncope; according to 2007 American College of Emergency Physicians (ACEP) Clinical Policy on Syncope.

KEY ASPECTS IN HISTORY

• The three main points on which the etiology of syncope can be determined are:– Precipitant Factors– Activity the patient was involved in before the

incident– Patient’s position

Precipitant Factors

• Fatigue• Food and water deprivation• Warm and ambient enviornment• Alcohol• Pain• Specific Phobias• Strong emotional stimuli such as fear and

appprehension

Activity prior to the episode

• If occurred at rest• Change in posture• On exertion / after exertion• Specific Situations:– Shaving, coughing, voiding or prolonged standing.

• If occurs within 2 minutes of standing denoted OH (Orthostatic Hypotension – Classical).

Position of the patient

• Whether the patient was standing, sitting, lying down when the syncope occurred.

• Syncope while sitting or lying down most likely is cardiac

Important Hx questions about the attack

• Was the loss of consciousness complete?• Was loss of consciousness with rapid onset

and short duration?• Was recovery spontaneous, complete, and

without sequelae?• Was postural tone lost?

Other associated complaints

• Prior faintness, dizziness, or light-headedness – denotes p/o syncope in 70 % of patients

• During pre syncopal period – – Vertigo, blurred or faded vision, pallor, or

paresthesias , diaphoresis – p/o syncope– Aura – p/o seizures

Some Red Flag Signs• These when present should prompt for further evaluation

of the patient• These includes:– Exertional onset– Chest Pain– Dyspnea– Low back Pain– Palpitations– Severe headache– FND (Focal Neurological Deficits)– Diplopia, ataxia or dysarthria

After episode

• Ask about the duration of loss of consciousness– If in seconds to minutes – p/o Syncope– If more than that – p/o Seizures

• After regaining consciousness, whether the patient was confused, had oral trauma, incontinence or myalgias.

• Post event confusion rare in syncope, and when it occurs, its always less than 30 seconds.

MEDICATION HISTORY

• Reduce BP - Anti-hypertensives, diuretics, nitrates• Affect Cardiac Output – Beta-blockers, digitalis,

antiarrythmics• Prolong QT-interval – TCAs, phenothiazidines,

quinine, amiodarone• Alter sensorium – Alcohol, cocaine, analgesics,

sedatives• Alter serum electrolytes - Diuretics

PAST MEDICAL HISTORY

• Cardiac Etiology– MI, Arrythmias, Structural cardiac diseases,

Cardiomyopathies, CHF, abdominal aortic aneurysm

• Neurological Etiologies:– H/o Seizure disorder, CVA, DVT

• Diabetes

PHYSICAL EXAMINATION

• VITALS:– Temperature : Fever – UTI or Pneumonia– Pulse: • Tachycardia – PE, Hypovolemia, tachyarrythmias or ACS• Bradycardia – Cardiac Conduction defects, ACS

– BP – for Orthostatic Hypotension– Glucose – Hypoglycemia

• Higher Functions:– Patients with genuine syncope should have a

normal baseline mental status– If confusion, abnormal behavior, headache, fatigue

or somnolence is present – p/o toxic, metabolic or CNS cause should be considered.

• Signs of Trauma-– Head injury, lacerations, extremity fractures– Tongue bite – p/o seizures

• Sos Carotid Sinus massage

Causes of Syncope


CAUSES OF SYNCOPE

• Reflex (Neurally-mediated) syncope NMS– Vasovagal

• Emotional stress, fear, pain, blood phobia, instrumentation• Mediated by orthostatic stress

– Situational• Cough, sneeze, • Gastrointestinal (swallow, defaecation, visceral pain)• Post-exercise• Post-prandial• Others (laugh, brass instrument playing, weightlifting)

Orthostatic Hypotension

• Fall in systolic BP by 20 mmHg or more and/or fall in diastolic BP by 10 mmHg or more or systolic BP to < 90 mmHg, when a person assumes a standing position from sitting or supine position.

• Classification– Initial OH ( 0 – 30 sec)– Classical OH (30 sec – 3 min)– Delayed (progressive) OH (3 – 30 min)– Delayed (progressive) OH + Reflex syncope (3 – 45 mins)

• Orthostatic hypotension– Primary autonomic failure• Pure autonomic failure, Parkinson’s disease with

autonomic failure, Lewy body dementia, multiple system atrophy

– Secondary autonomic failure• Diabetes, amyloidosis, uremia, spinal cord injures

– Drug-induced orthostatic hypotension• Alcohol, vasodilators, diuretics, antidepressants

– Volume depletion• Haemorrhage, diarrhoea, vomitting


• Cardiac Syncope– Arrythmias as primary cause:• Bradycardia:

– Sinus node dysfunction – AV conduction disease– Implanted device failure

• Tachycardia– Supraventricular– Ventricular (idiopathic, secondary to structural heart diseases,

channopathies)• Drug induced tachycardia and bradycardia

• Cardiac Syncope– Structural disease (Cardiac)• Valvular heart disease, Acute MI/ischemia, HOCM,

Cardiomyopathy, Cardiac Mass (Atrial Myxomas, tumors),• Pericardial diseasea/tamponade, congenital anomalies

of coronary arteries, prosthetic valve dysfunction– Structural disease (Extra cardiac)• Pulmonary embolus, acute aortic dissection, pulmonary

hypertension


CONDITIONS MISDIAGNOSED AS SYNCOPE

• With partial or T-LOC w/o global cerebral hypoperfusion– Epilepsy– Metabolic disorders including hypoglycemia, hypoxia,

hyperventilation with hypocapnia– Intoxications– Vertebrobasilar TIA

• W/O impairment of consciousness– Cataplexy– Drop attacks– Falls– Functional (psychogenic peudosyncope)– TIA of carotid origin

RISK STRATIFICATION

• SAN FRANCISCO SYNCOPE RULE (SFSR)– Abnormal ECG– Congestive Cardiac Failure– Shortness of breath – Haematocrit < 30%– SBP < 90 mmHg

• No risk :: score = 0• Risk of serious events in 7 days :: score >= 1

DIAGNOSTIC TESTS

ECG

• ECG is most important investigation which helps suffice the diagnosis in most of the situations

• If that does not help then, International Study On Syncope Of Unknown Etiology (ISSUE) investigators advise some further tests.

Carotid Sinus Massage

• Indicated in patients > 40 years of age with syncope of unknown etiology after initial evaluation

• Contraindicated in patients with previous TIA or stroke in prior 3 months and in patients with carotid bruits

• RESULT: Diagnostic if syncope is reproduced in the presence of asystole longer than 3 seconds and/or fall in SBP > 50 mmHg

CAROTID SINUS MASSAGE (CSM)

ACTIVE STANDING

TILT TABLE TESTING

Interpretation Of Tilt Table Test (TTT)

VASIS CLASSIFICATION• Type 1 – Mixed. Both HR and BP are reduced. BP reduction

precedes HR reduction. HR reduction >10% but never < 40 / min• Type 2 – Cardioinhibitory. Reduction in both HR and BP. BP

decrease precedes HR reduction. Minimum HR is < 40/min or ayatole > 3sec

• Type 3 – Pure vasodepressor. HR does not decrease to more than 10%

• Chronotrophic incompetence - no HR increase in spite of the tilt• Excessive HR rise – POTS (Positional Orthostatic Tachycardia

Syndrome)

Reproduced from: Journal of American College Of Cardiology

ELECTROCARDIOGRAPHIC MONITORING

• Conventional Ambulatory Holter Monitoring• In-Hospital Monitoring• Event Recorders• External or implantable loop recorders• Remote (at home) telemetry

In-Hospital Monitoring

• Indicated only when the patient is at high risk of a life-threathening arrythmia

• To be applied immediately after syncope, for a few days, to look for arrhythmic syncope

• Yield only 16%

Holter Monitoring

• Conventional 24 – 48 hour, or even 7 days, Holter recorders.

• Yield may be as low as 1 – 2 %

External Loop Recorders

• These devices have a loop memory which records and deletes ECG

• When activated by the patient typically after the event, they records and saves the pre-activation 5 – 15 minutes of ECG.

• Very less useful in infrequent syncope and requires high patient compliance

Implantable Loop Recorders (ILRs)

• Life span of 36 months• Solid state loop memory that stores

retrospective ECGs when activated by bystander or patient, usually after a syncopal episode, or automatically in case of an occurrence of predefined arrythmias.

Reproduced From: http://openi.nlm.nih.gov/

Reproduced From: Hall-Garcia Cardiology, Texas

Remote (at home) Telemetry

• External and implantable device systems are available that are able to provide continuous ECG recording or 24 hour loop memory, with wireless transmission (real time) to a service center.

ELECTROPHYSIOLOGICAL STUDY (EPS)

Echocardiography

• For patients suspected of having a structural heart disease

Psychiatric Evaluation

• Various psychiatric drugs can precipitate syncope through OH and prolonging QT interval

• However, disruption of anti psychotic medications may have severe psychiatric consequences

• These patients may present with “Functional Attacks” of T-LOC

• Functional Attacks– Pseudoseizures– Pseudosyncopes

NEUROLOGICAL INVESTIGATIONS

• Electroencephalogram• CT/MRI• Neurovascular Studies– Doppler USG

TREATMENT

• Principal goals:– Prolong survival– Limit physical injuries– Prevent recurrences

TREATMENT OF REFLEX SYNCOPE

• Lifestyle modifications– Aviodance of possible triggers– Early recognition of prodromal symptoms– Performing maneuvers to abort the episode• Supine position• Physical counterpressure maneuvers (PCMs)

Pharmacological considerations

• α – agonists– Midodrine

• Fludrocortisone– Some benefits in adults with reflex syncope

• β – blockers• Paroxetine

Individual considerations

• For VVS– Tilt table testing• To make patients familiarize with prodromal symptoms

– PCMs (Physical Counterpressure Maneuvers) • For Situational Syncope• Carotid Sinus Syncope– Dual Chamber Cardiac Pacing

ORTHOSTATIC HYPOTENSION & OTHROSTATIC INTOLERANCE

• Principal Goals– Expansion of ECF volume

• In absence of hypertension, patient instructed to take sufficient salt and water intake (target 2 – 3 litres and 10 gm NaCl)

• Rapid cool water ingestion– Orthostatic intolerance and post prandial

hypotension

• Sleeping with head end of bed elevated (10◦)• For gravitational venous pooling– Abdominal binders or compressive stocking

• Pharmacological – Midodrine– Fludrocortisone

Other treatment Modalities

• Octreotide– Post prandial hypotension

• Erythropoetin– Anaemia

• Pyridostigmine• Frequent small meals• Judious use of leg and abdominal muscles

CARDIAC CAUSE - TREATMENT

• Treat the underlying cause

Syncope in the elderly

• Most common cause of syncope are OH, reflex syncope (especially CSS) and cardiac arrythmias

• Syncope in morning favors OH• Taking multiple medications, whose

withdrawal/overdose leads to syncope

• OH is not always repeatable in the elderly (particularly medication and age related). Therefore, orthostatic BP appraisal should be repeated, preferably in the morning and/or promptly after syncope

• CSM is particularly important• Tilt testing is well tolerated and safe• Twenty-four hour ambulatory BP recordings may be

helpful if instability of BP is suspected• Due to high frequency of arrythmias, an ILR may be

especially useful in elderly with unexplained syncope

Driving and Syncope

• In a large study, 9.8 % had syncope while driving, which was commonly reflex (37 %) or cardiac (12%)

• The cumulative probability was only 7 % in 8 years

• Risk of syncope mediated driving accidents was 0.8% per year

Refereneces

• eMedcape Website• European Society Of Cardiology (ECS); European

Heart Journal• www.dizziness-and-balance.com• Harrison’s Textbook Of Internal Medicine 17th Edition• Merck Manuals (MSD – online)• American Heart Journal• PubMed (National Institute Of Health –NIH)• Mayo Clinic websites

http://www.dizziness-and-balance.com/

Dr. Tikal KansaraIInd Year Resident

SSG Hospital & Medical College, Vadodara

Health & Medicine

Syncope