SYNCOPE

Dr. Renuka Rayana

1st year PG
MIMS
 DEFINITION
— Transient self-limiting loss of consciousness with
loss of postural tone due to acute global
impairment of cerebral blood flow.
— Sudden onset.
— Brief duration.
— Spontaneous & complete recovery.
— Without neurological deficit.
— Without requiring resuscitation.
 EPIDEMIOLOGY
— 3% of emergency visits.

— 6% of medical admissions.

— 1% of all hospital visits.

— Peak age group in young between 10-30yrs.

— Incidence increases after 70yrs in elderly.

— Common in females.

— Young often have family history in 1st degree

relative.
 PRESYNCOPE
— Prodromal of syncope.

— May occur with out any warning symptoms.

Typical symptoms are:

— Dizziness, lightheadedness or faintness,

weakness, fatigue, and visual and auditory
disturbances.
— Normal cerebral blood flow is 50-
60ml/min/100gm of brain tissue.

— Cessation of blood flow for 6-8sec causes

loss of consciousness i.e. when blood flow
decreases to 25ml/min/100gm of brain tissue.
 CEREBRAL PERFUSION
PRESSURE
CPP defined as the MAP minus the ICP, provides
the driving force for circulation across the
capillary beds of the brain.

CPP = MAP-ICP

MAP = DBP+1/3PP

• CBF remains constant with a CPP of 50-

150mmHg.
 AUTOREGULATION
— Autoregulation is the physiological response
by which cerebral blood flow is regulated.
It depends on:

— Cerebral blood flow.

— Metabolic causes like viscosity, temperature,

PCO2, PH, PO2.
Autoregulation is a myogenic mechanism,
vascular smooth muscle constricts in
response to an increase in wall tension and
relax to a decrease in wall tension.

Systemic BP increases

Vasoconstriction of cerebral vessels

Prevents hyper perfusion

— CBF increases with hypercapnia and acidosis.

— CBF decreases with hypocapnia and alkalosis.

PATHOPHYSIOLOGY OF
SYNCOPE
On Standing

500-1000ml of Blood Pooling in LL &

Splanchnic Circulation

Decrease Venous return

Decrease Ventricular filling
Decreased CO & BP

Compensatory Baroreceptor Reflex

THE BARORECEPTOR REFLEX
If this response fails, as is the case chronically
in orthostatic hypotension and transiently in
neurally mediated syncope, cerebral
hypoperfusion occurs.
The causes of syncope can be divided into:

— Neurally mediated syncope (also called

reflex syncope).

— Orthostatic hypotension.

— Cardiac syncope.
NEURALLY MEDIATED SYNCOPE
Sudden transient change in autonomic efferent
activity

Increased parasympathetic outflow &

Sympathoinhibition

Bradycardia, vasodilatation, fall in BP

Reduce CBF below the lower limit of autoregulation

Syncope
— Vasovagal syncope is provoked by emotions,
pain, stress.

— In situational syncope specific localized

stimuli provoke vasodilatation & bradycardia.

— Hyperventilation causes hypocarbia, cerebral

vasoconstriction & raised intra thoracic
pressure decreases the venous return.
 TREATMENT OF
VASOVAGALSYNCOPE
— Reassurance & avoid provocative stimuli.

— Plasma volume expansion with fluid & salt.

— Isometric counter pressure maneuvers like

handgrip, leg crossing.

— In refractory cases fludrocotisone & beta

adreno receptor blockers are used.
ORTHOSTATIC HYPOTENSION
— Reduction in SBP of at least 20 mmHg or DBP
of at least 10 mmHg within 3 minutes of
standing or head-up tilt on a tilt table, is a
manifestation of sympathetic vasoconstrictor
(autonomic) failure.

— Orthostatic hypotension occurs within 15

seconds of standing ("initial" orthostatic
hypotension).
ORTHOSTATIC HYPOTENSION
— It represents a transient mismatch between
cardiac output and peripheral vascular
resistance and does not represent
autonomic failure.
 SYMPTOMS
— Characteristic symptoms include headache,
dizziness, presyncope.
— Others include Visual blurring, Neck pain —
typically in
- Suboccipital
- Posterior Cervical
- Shoulder region) (coat-hanger headache
— Symptoms may be aggravated with increased
temperature, prolonged standing, exercise, after
heavy meals & drugs.
 TREATMENT
— Remove the reversible causes like any drugs.

— Isometric maneuvers.

— Increased fluid & salt intake.

— Fludrocortisone acetata, midodrine, l-

dihydroxy serine & pseudoephedrine can be
used.

— Additional theraphy with pyridostigmine,

yohimbine, DDAVP & EPO.
ANS FUNCTION TESTS
Heart rate response to deep breathing
(HRDB):
— During 6 maximum deep breaths PR
falls>15beats/min-normal.
— Autonomic disturbance PR slows<10beats/min.
Valsalva ratio:
— Highest PR/Lowest PR: >1.5 - normal.
— Autonomic diturbance: <1.1
TST: Sweat production in response to
elevation in body temp.

— QSART & TST- absent sweating – post

ganglionic lesion.

— QSARTis normal & TST shows anhidrosis-

preganglionic lesion.
ORTHOSTATIC BP:
Lies down for 15 min-check BP

stands – PR at 15th & 30th beat

BP after 1min & 3rd min
Normal SBP doesn’t fall >10mmhg
Autonomic dysfunction SBP falls by >30mmhg
30th beat to 15th beat PR ratio: >1.03 normal
<1.0 in autonomic dysfunction
 CARDIAC SYNCOPE
— It is caused by arrhythmias and structural
heart diseases.
Bradyarrhythmias:
— Sino atrial block.
— AV block(mobitz 2, complete AV block).
— Verapamil/beta blocker therapy.
Syncope due to bradycardia or asystole is
known as stokes-adams attack.
Tachyarrhythmias:

— Ventricular tachycardia it’s the most

common cause of cardiac syncope.

— SVT.

— Inherited channelopathies like long QT

syndrome, brugadas, PMVT.
Structural defects of heart:
— Severe AS.
— HOCM.
— Atral mxomas.
— Pericardial effusion.
— MI.
— Cardiomyopathies.
Hyper/hypo kaemia, renal failure, ventrical
aneurysms will predispose to arrhythmias.
 TREATMENT
— Treatment of cardiac disease depends upon
the underlying disorder.

— Therapies for arrhythmias include cardiac

pacing for sinus node disease and AV block,
and ablation, anti-arrhythmic drugs, and
cardioverter-defibrillators for atrial and
ventricular tachyarrhythmias.
 High-Risk Features Indicating
Hospitalization of Syncope

— Chest pain suggesting — Persistent sinus

coronary ischemia. bradycardia.
— Features of congestive — Trifascicular block.
heart failure.

— Moderate or severe — Atrial fibrillation.

valvular disease.

— Moderate or severe — Nonsustained ventricular

structural cardiac disease. tachycardia.

— Electrocardiographic — Family history of sudden
death
features of ischemia

— History of ventricular — Preexcitation syndromes

arrhythmias

— Prolonged QT interval — Brugada pattern on ECG

(>500 msec)

— Repetitive sinoatrial block

or sinus pauses
APPROACH TO SYNCOPE
History:
— We should focus on the events preceding
following the syncopal attack.
— Prodromal symptoms.
— Provoking stimuli.
— Any triggers, chest pain.
— Level of consciousness.
— Associated with exertion.
— Association with fecal incontinence,
seizures, confusion, disorientation.

— Associated with hunger, tremors, ataxia,

vertigo.

— Preceding history of palpitations.

— H/o drug intake like beta blockers,

verapamil, anti arrhythmics, diuretics.
— h/o cardiac, renal diseases, DM, htn, alcohol

— h/o trauma

— Family history and past history

Physical examination:
Vitals: PR-arrhythmia

BP-postural hypotension & other vitals

• Tongue bite, head trauma, carotid bruit

• ANS tests
• CVS and CNS examination
— Investigations: Hb, Rbs, pottasium,
bicarbonate and routine investigations.

— ECG-abnormal then ECHO, Holter

monitoring, EPS.
DIFFERENTIAL DIAGNOSIS
— Hypoglycemia-hunger, tremor, palpitations,
parasthesias.
— Cataplexy-loss of muscle tone with
consciousness preserved.

— Vestibular dysfunction, cerebellar diseases,

psychiatric disorders, TIA.
Thank you
 REFERENCES
— HARRISON'S PRINCIPLES OF INTERNAL
MEDICINE 19th EDITION
— CLINICAL METHODS IN CARDIOLOGY
B.SOMARAJU

— WASHINGTON MANUAL OF MEDICAL

THERAPEUTICS