Syncope

The dizzy and woozy world

Syncope: Definition
a syndrome in which loss of consciousness is: relatively sudden, temporary, self-terminating usually rapid recovery due to inadequate cerebral perfusion, most often triggered by a fall in systemic arterial pressure

Syncope is only one of many conditions that cause transient loss of consciousness (TLOC)

Transient Loss of Consciousness

Trauma-induced Not Trauma-induced Not True TLOC

Concussion

Syncope Seizures Intoxications Metabolic disorders

TLOC mimicks, without true loss of consciousness e.g.,

psychogenic pseudosyncope drop attacks cataplexy

Syncope:
A Symptom, Not a Diagnosis
Self-limited loss of consciousness and postural tone Relatively rapid onset Variable warning symptoms Spontaneous, complete, and usually prompt recovery without medical or surgical intervention

Underlying mechanism: transient global cerebral hypoperfusion.

Section 2:
Classification, Prevalence, Social & Economic Impact

Causes of True Syncope

NeurallyMediated Reflex
1
VVS CSS Situational Cough Postmicturition

Orthostatic

Cardiac Arrhythmia

Structural CardioPulmonary
4 Aortic Stenosis HCM Pulmonary Hypertension Aortic Dissection

2 Drug-Induced ANS Failure Primary Secondary

3 Bradycardia Sinus pause/arrest AV block Tachycardia VT SVT LongQT Synd

60%

15%

10%

5%

Unexplained Causes = Approximately 10%

Syncope Mimics:
Real or Seemingly Real TLOC not due to Cerebral Hypoperfusion

Acute Intoxication (e.g., alcohol) Seizures Sleep disorders Somatization disorder

psychogenic pseudo-syncope

Trauma/concussion Hypoglycemia Hyperventilation

Syncope:
Epidemiological Data

40% population, presumed syncope at least once1

1-6% of hospital admissions2

Approx 1% of ED visits per year3,4 10% of falls by elderly are believed due to syncope5 Injuries:

6% major morbidity (e.g., fractures, MVA)1 Minor injury in 29%1

1Kenny

RA, et al. eds. The Evaluation and Treatment of Syncope. Futura;2003:23-27. 2Kapoor W. Medicine. 1990;69:160-175.

3Brignole 4

M, et al. Europace. 2003;5:293-298. Blanc J-J, et al. Eur Heart J. 2002;23:815-820. 5Campbell A, et al. Age and Ageing. 1981;10:264-270.

Impact of Syncope on Mortality Risk

Vasovagal Syncope has low mortality risk
But recurrences are a concern

Syncope of presumed cardiac cause is associated with high mortality risk

Most evidence suggests that risk is similar to that of patients without syncope but with similar severity of heart disease

Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med. 2002;347(12):878-885. [Framingham Study Population]

Syncope
Electrical Problems Motor Problems Valve Stenosis Problems Fuel System Issues. Clots and such Supply and demand Issues Hemodynamic instability Homeostasis

Syncope
Catecholamine Disorders Central Autonomic Disorders Orthostatic Intolerance Syndrome Paroxysmal Autonomic Syncope Peripheral Autonomic Disorders

Neurocardiogenic Syncope
Orthostatic hypotension Orthostatic hypotension is defined as a drop of 20 mm Hg in systolic blood pressure and 10 mm Hg diastolic blood pressure on standing, associated with typical symptoms.

Syncopal attacks in children

20% of children will have a syncopal episode before the age of 15 years. More than 70% are due to neurally-mediated reflex responses and vast majority are benign. Benign Vasovagal Syncope (simple faints) and Reflex Anoxic Seizures aka- Reflex Asystolic Syncope. Both conditions are benign, upsetting for both the child and the parents. Careful history taking is the key to diagnosis.

Situational syncope
A type of vasovagal syncope that occurs only during particular situations that cause unusual patterns of stimulation to certain nerves. The stimulus that triggers an exaggerated neurological reflex can be a wide range of different events. Dehydration, intense emotional stress, anxiety, fear, pain, hunger or use of alcohol or drugs.

Situational syncope
Syncope may also occur immediately after peak exercise. This contrasts with collapses occurring during exercise, for example if the person has aortic stenosis. The cause is thought to be due to vasomotor center dysfunction.

Situational syncope
Hyperventilation associated with panic or anxiety. Cough syncope. Carotid sinus hypersensitivity (turning the neck or wearing a tight collar). Micturition syncope.

Psychogenic syncope
Sometimes syncope may be feigned. This is known as Psychogenic syncope.

Neurologic syncope:
Loss of consciousness due to a neurological conditions. Seizure. Strokes, transient ischemic attacks. Migraines. Normal pressure hydrocephalus. Sleep disorders

Cardiac syncope:
Loss of consciousness due to cardiovascular conditions that interferes with blood flow to the brain. Arrhythmia. Asystole. Conduction issues. Obstructed blood flow in the heart or blood vessels, valve disease, aortic stenosis, blood clot, or heart failure.

Syncope: Carotid Sinus Syndrome

Carotid sinus hypersensitivity. Carotid sinus massage causes a three second, or longer, pause in the heart beat (cardio inhibition). Drop blood pressure by 50 mm Hg. or more (vasodepression). 56% of cases of unexplained syncope are found to have Carotid sinus hypersensitivity.

Postural syncope
Postural hypotension: occurs when the blood pressure drops suddenly due to a quick change in position, such as from lying down to standing. Postural syncope can be related to certain medications or intravascular volume depletion due to bleeding, dehydration or vasomotor instability.

Vasovagal syncope
When you stand up, gravity causes blood to settle in the lower part of your body, below the level of the diaphragm. In response, the heart and autonomic nervous system (ANS) react to maintain your blood pressure. These physiologic responses can be exaggerated or abnormally blunted.

Vasovagal syncope
Vasovagal syncope may occur with orthostatic hypotension. The blood vessels do not constrict normally when the patient stands, causing blood to pool in the legs and the blood pressure to drop quickly.

Section 3:

Diagnostic Strategy

The Initial Evaluation: 4 Key Questions

Did the patient suffer true Transient Loss of Consciousness (TLOC)?
Was TLOC due to syncope or some other cause?

Is heart disease present?

Does the medical history (including observations by witnesses) suggest a specific diagnosis?

Diagnosis
Careful review of medical history and a physical exam. Detailed questions about symptoms and syncope episodes. Premonitory symptoms and the circumstances in which symptoms occur.

Diagnosis
Medication history Bleeding disorders Seizure disorders Migraine Infections GI symptomtology

Diagnosis
ECG Echocardiogram Holter monitor Long term event recorder Implantable loop recorder Electrophysiology study

Diagnosis
Sick Sinus Syndrome AV Nodal disease Infra His Disease Tachyarrhythmia Blood sugar measurements Carotid Doppler and ultrasound EEG

Diagnostic Goal

Establish cause of syncope with sufficient certainty to: Assess prognosis confidently Initiate effective preventive treatment

A Diagnostic Plan is Essential

Initial Examination
Detailed history & Physical exam (Supine/Standing BP) ECG, possibly Echocardiogram

Risk Assessment
In-hospital vs Out-of-hospital Diagnostic evaluation Presence of Structural Heart Disease (SHD) vs None

Selected Testing Based on Initial Exam & Risk

Ambulatory ECG Monitoring (Event-monitor, MCOT, ILR) Hospital-based Hemodynamics / Angio, StressTesting, EPS, Tilt-table

A Diagnostic Plan is Essential

Modified after ESC Syncope Task Force, 2004

Initial Examination: Essential Elements of the History

Circumstances of recent event(s)
Eyewitness account of event Symptoms at onset of event (warning symptoms)

Sequelae

Concomitant disease, especially cardiac

Medication history

Pertinent family history

Cardiac disease, Sudden death Metabolic disorders

Past medical history

Neurological history Syncope

Clinical Features Suggesting Cause of Syncope

ESC Syncope Task Force 2004 Neurally-mediated Reflex Syncope
Absence of cardiac disease (except CSS) Long history of recurrences Associated with emotional event, pain, prolonged upright posture, hot environment, head rotation After strenuous exertion Associated with change to upright posture, prolonged standing, dehydration Recent addition of diuretic, vasodilator, etc History of neuropathy, diabetes, alcohol abuse Definite structural heart disease, acute cardiac ischemia Family history of sudden death Occurred during exercise ECG evidence of prior MI, acute ischemia, AV block, long QT, preexcitation, etc

Orthostatic Syncope

Cardiac Syncope

CSS=carotid sinus syndrome

Syncope Risk Stratification:

Is in-hospital evaluation needed?

Primary concerns:
Is there an immediate mortality risk? Is physical injury (e.g., falls risk) likely? Does treatment require in-hospital monitoring?

Currently many syncope patients undergo in-hospital evaluation

Admission rate in US is ~36%

Many admissions could be avoided by:

Better risk stratification Availability of syncope management units

Hospital Admission for Diagnosis or Treatment

Strongly recommended for diagnosis
Suspected or known significant heart disease ECG abnormalities suggestive of arrhyhmic syncope

Syncope during exercise, Syncope causing severe injury

Family history of sudden death

Strongly recommended for treatment

Cardiac arrhythmias, Syncope 2 structural cardiac or cardiopulmonary diseases When a pacemaker implantation is planned

Occasionally may need to be admitted

No heart disease but sudden onset of palpitations shortly before syncope or high suspicion of cardiac syncope Syncope in supine position, Frequent recurrent episodes
ESC Syncope Task Force 2004

Test to determine causes of syncope

Head-up tilt test Blood volume determination: Hemodynamic testing: Autonomic reflex testing: Sleep study (Polysomnogram)

Initial Examination:
Essential Elements of the Physical Examination
Vital signs
Heart rate, regularity
Orthostatic blood pressure change

CV Exam: Is heart disease present?

ECG: Long QT, WPW, conduction system disease Echo: LV function, valve status, HCM

Neurological exam
Residual deficits?

Carotid sinus massage

Perform under clinically appropriate conditions preferably during tilt-table test. Monitor BP

Carotid Sinus Massage (CSM)

Method
Massage, ~10 seconds, firm but do not occlude Supine and upright posture (on tilt-table)

Suggests Carotid Sinus Syndrome (CSS) if:

>3 sec asystole and/or >50 mmHg fall in systolic BP Or Reproduction of symptoms (usually only occurs with CSM during upright posture)

Sutton R, Benditt DG , In The Evaluation and Treatment of Syncope: A Handbook for Clinical Practice, 2005

Carotid Sinus Massage (CSM)

Relative contraindications Carotid bruit Pre-existing clinically significant carotid arterial disease CVA within previous 3 months Acute MI within previous 3 months Complications Transient neurological symptoms Less than 0.2%
Sutton R, Benditt DG , In The Evaluation and Treatment of Syncope: A Handbook for Clinical Practice, 2005

Additional Diagnostic Tests - 1:

Selected Use Based on Initial Examination and Risk Stratification
Ambulatory ECG
Holter Monitoring Typical Event Recorder External MCOT Loop Recorder Records & transmits ECG data with / without patient activation Insertable Loop Recorder ** Permits remote downloading Wireless transmission in certain devices

** Highest diagnostic yield for infrequent symptom events

Additional Diagnostic Tests - 2:

Selected Use Based on Initial Examination and Risk Stratification
Head-Up Tilt Test (usually combined with CSM) Electrophysiology Study (EPS) Non-invasive Risk Stratification for Life-threatening ventricular tachyarrhythmias
SAECG HRV HR turbulence Microvolt Twave alternans

Generally exhibit high negative predictive value but low positive predictive value

Heart Monitoring Options

Syncope Occurs Infrequently, Long-term Monitoring is Likely to be Most Effective

12-Lead Holter Monitor

10 Seconds

2 Days

Typical Event Recorder

MCOT External Loop Recorder ILR

7 Days

30+ Days

36 Months

ILR = insertable loop recorder MCOT= mobile cardiac outpatient telemetry

External Mobile Cardiac Outpatient Telemetry (MCOT) ECG Recorder

Patient Indicates symptoms on PDA. Abnormal ECG transmitted automatically PDA stores ECG data and symptom status. Wireless transmission capability provided.

Physician receives and acts upon data as medically appropriate

Monitor center receives, reviews and transmits data to physician. Pre-determined urgency criteria determine timing of physician alerts

Cardionet Inc., San Diego, CA

Insertable Loop Recorder (ILR)

An ECG monitoring system that is implanted subcutaneously
Capable of recording, storing, and if necessary remotely transmitting ECG signals
Patient-activated and/or automatically-activated Longevity of current ILRs up to 36 months

Indicated for
Patients with unexplained syncope / TLOC Patients who experience transient symptoms that may suggest a cardiac arrhythmia Patients at increased risk of cardiac arrhythmias

Symptom-Rhythm Correlation:
ILR Permits both Patient-triggered and Automatic Activation

Auto Activation Point

Patient Activation Point

ILR Symptom-Rhythm Correlation:

Case Examples

Case: 56 year old woman with refractory syncope accompanied with seizures.
*Medtronic data on file

Case: 65 year old man with syncope accompanied by brief retrograde amnesia.

 Protocols vary Performed with or without provocative drugs Goals:

Head-Up Tilt Test (HUT)

Unmask VVS susceptibility Reproduce symptoms Patient learns VVS warning symptoms Patient more confident of diagnosis

Not useful for predicting treatment benefit

VVS: Typical HUT Protocols - 1

Basic Preparation 4 hour fast Continuous ECG monitor Continous BP monitor

Finapress or equivalent preferred Arterial line, if placed >1 hour before Sphygmomanometer discouraged

ESC Syncope Task Force 2004

VVS: Typical HUT Protocols - 2

Tilt Procedure
Tilt to 60- 70, 20 min Positive end-point: Syncope If negative, then drug provocation
Nitroglycerine 0.4mg SL, or Isoproterenol 1-5 mcg/min, to increase Heart Rate to 125% baseline

Repeat tilt, duration 10 minutes

ESC Syncope Task Force 2004

Induction of VVS by Upright Posture

Cardioinhibitory & Vasodepressor Components

From Wieling W et al.(with permission)

Neurological Tests for TLOC:

EEG, Head CT / MRI

Not useful for syncope evaluation

Imaging may be warranted if there is concern about head injury from fall May be useful in non-syncope TLOC patients but neurological consultation is advised prior to tests

Neurological Tests for TLOC:

EEG, Head CT, Head MRI

Test

PATIENTS (N=433)

YIELD

History & Physical Examination

140

32%

ECG
EPS GXT Carotid Massage Cardiac Catheterization Cerebral Angiography Electroencephalogram
1Kapoor 2Linzer

30
7 2

7%
2% 0.5% 46%2

11 2 2

3% 0.5% 0.5%

W, Medicine. 1990;69:160-175. M, et al. Ann Intern Med. 1997;127:76-86.

Treatment
Treatment is aimed at preventing a syncope recurrence Taking new medications or making changes to your current medications Wearing support garments or compression stockings to improve circulation

Treatment
Making certain dietary changes such as eating small, more frequent meals; increasing salt, fluid and potassium; and avoiding caffeine and alcohol Taking certain precautions when changing positions from sitting to standing Proamitine, Florinef, Sudafed,Nadolol

Treatment
Elevating the head of your bed while sleeping. Avoiding or changing the situations or "triggers" that cause a syncope episode Biofeedback training to control a rapid heartbeat.

Treatment
Pacemaker implantation to regulate the heart rate -- only as needed for certain medical conditions Implantable cardiac defibrillator (ICD), which constantly monitors your heart rate and rhythm and corrects a fast, abnormal rhythm -- only as needed for certain medical conditions

Treatment
About 30 percent of people with one episode of syncope will have a recurrence. The underlying cause of syncope and the patient's age, gender and presence of other medical conditions will affect the prognosis or outlook.

Central Autonomic Disorders

Multiple System Atrophy - Shy Drager Syndrome Parkinson's Disease

Orthostatic Intolerance Syndrome

Postural Tachycardia Syndrome (POTS) Mitral Valve Prolapse Idiopathic Hypovolumia Paroxysmal Autonomic Syncope

Neurocardiogenic Syncope

Peripheral Autonomic Disorders

Acute Idiopathic Polyneuropathy Guillain Barr Syndrome Chagas' Disease Diabetic Autonomic Failure Familial Dysautonomia Pure Autonomic Failure

Catecholamine Disorders
Baroreflex Failure Dopamine -- Hydroxylase Deficiency Pheochromocytoma Neuroblastoma Chemodectoma Familial Paraganglioma Syndrome

Catecholamine Disorders
Tetrahydrobiopterin Deficiency Aromatic L-Amino Acid Decarboxylase Deficiency Menkes Disease Monoamine Oxidase Deficiency States Disorders of Dopamine Metabolism

Autonomic reflex testing

QUANTITATIVE PSUDOMOTOR AXON REFLEX TESTING (QSART) QSART offers quantitative measurement of axon reflex-mediated sudomotor (sweat) responses and the evaluation of postganglionic sympathetic small nerve fibers. Measurements are taken at four skin sites on the upper and lower extremities.

RESTING SWEAT TESTING

This test measures the amount of sweat produced while the body is at rest as another index of activity of small nerve fibers. During testing, the patient lies quietly and is usually very comfortable. VASOMOTOR TESTING Skin temperatures at various sites on the arms and legs is recorded using a highly sensitive thermometer.

EVALUATION OF CARDIAC-VAGAL AND ADRENERGIC FUNCTIONS

DEEP BREATHING: This is one of the most reliable cardiovascular heart rate tests for evaluating autonomic function and measures heart rate responses to deep slow breathing.

VALSALVA MANEUVER
This test mimics everyday activities which require heavy lifting or straining, that may result in lightheadedness or even loss of consciousness. During the Valsalva maneuver, the patient is asked to exhale steadily into a bugle for 15 seconds at 40 mmHg while in the supine position.

TILT TABLE TEST

Current standardized tilt protocols possess the sensitivity and specificity to identify individuals with pre-syncope, syncope, and orthostatic hypotension. Tilt table testing evaluates beat-to-beat heart rate and blood pressure, respiration and carbon dioxide responses to passive standing.

QUANTITATIVE SENSORY TESTING Quantitative sensory testing evaluates sensation of vibration, cold, warm, heat, and pain. It can be used for the patients with chronic pain.

Neurology testing
ELECTROENCEPHALOGRAPHIC MONITORING (EEG) TRANSCRANIAL DOPPLER MONITORING (TCD)

TCD enables noninvasive monitoring of cerebral blood flow from intracranial vessels for evaluation of vasospasm, stroke and migraine headache.

24-HOUR ABP MONITORING

Enables noninvasive ambulatory monitoring of blood pressure over the period of 24 hours