APPROACH TO PATIENTS

WITH PRESYNCOPE AND

SYNCOPE
Yusuf Emre Gürel, Assoc Prof
Department of Cardiology
Marmara University School of Medicine

1
 Syncope (Greek – to interrupt)
• Syncope is the sudden
transient loss
0 of
0
consciousness and postural
tone with spontaneous
recovery.
• Loss of consciousness
occurs due to 10 seconds of
hypoperfusion of the
reticular activating system in
the mid brain.

2
 DEFINITION
• Transient loss of
consciousness with loss of
postural
EE tone.

– Sudden onset
– Brief duration
– Spontaneous & complete
recovery
– Without neurological
deficit
– Without requiring
resuscitation

!f!trequ!res
!t !s not syncope 3
 DEFINITION
• A syncopal prodrome (presyncope) is
common, although loss of consciousness may
occur without any warning symptom.
• Typical presyncopal symptoms:
üdizziness, F

ülightheadedness or faintness
üweakness, fatigue
0 and auditory
üvisual 0 disturbances.

4
 Maintenance of Postural
Normotension
• Standing à pooling of 500–1000 mL of blood in the lower extremities
and splanchnic circulation.
1
Ø decrease in venous return 1
Ø reduced ventricular filling
!
Ø diminished cardiac output and blood
pressure.
rare
• These hemodynamic changes provoke a
Freya
Ø compensatory reflex response
(baroreceptors)
Ø increase in sympathetic outflowgand
decrease in vagal nerve activity

a!me
Ø increase in peripheral resistance, venous
If
return to the heart, and cardiac output and
thus limit the fall in blood pressure.
5
 Classification of Transient Loss
of Consciousness (TLOC)
Real or Apparent TLOC

Syncope Disorders Mimicking Syncope

– Neurally-mediated (reflex) – With loss of consciousness, i.e.,
syncope seizure disorders, concussion
– Orthostatic hypotension – Without loss of consciousness, i.e.,
– Cardiac arrhythmias psychogenic “pseudo-syncope”
– Structural cardiovascular
disease

Brignole M, et al. Europace, 2004;6:467-537.

6
 Causes of True Syncope
Structural
Neurally- Cardiac
Orthostatic Cardio-
Mediated Arrhythmia
Pulmonary

1 2 3 4
• Brady
8
• VVS • Drug-Induced • Acute
• CSS carot!d
>
-
s!nus
syncope • ANS Failure ØSN Myocardial
Dysfunction Ischemia
• Situational ØPrimary
ØAV Block • Aortic
ØCough ØSecondary
• Tachy Stenosis
ØPost- 0
ØVT • HCM hypertroph!c card!othe
Micturition
ØSVT • Pulmonary
• Long QT Hypertension
Syndrome • Aortic
Dissection

Unexplained Causes = Approximately 1/3

DG Benditt, MD. U of M Cardiac Arrhythmia Center
7
 Syncope Mimics
• Acute intoxication (e.g., alcohol)
• Seizures (epilepsy) mostcommonm!m!cker

• Sleep disorders
• Somatization disorder (psychogenic pseudo-
syncope)
• Trauma/concussion
• Hypoglycemia
• Hyperventilation
• Transient ischemic attack
8
 Causes of Syncope by Age
pusually ben!gn
Younger Patient Older Patient
0
• Vasovagal
• Situational
• Cardiac**
Ben!gn – Mechanical
• Psychiatric – Arrhythmic
• Long QT*
• Orthostatic hypotension

EE
• Brugada syndrome*
• Drug-induced
• WPW syndrome*
• 1Neurally mediated
• RV dysplasia*
• Multifactorial
• Hypertrophic cardiomyopathy*
• Catecholaminergic VT
• Other genetic syndromes

9
.
 3 General Categories
• Neurally mediated (also called reflex syncope)
– transient change in the reflexes responsible for
maintaining cardiovascular homeostasis.
– Episodic vasodilation (or loss of vasoconstrictor tone) and
bradycardia occur in varying combinations, resulting in
temporary failure of blood pressure control.
a
e

• Orthostatic hypotension due to autonomic failure:

– cardiovascular homeostatic reflexes
0 are chronically
impaired. attrans!ent

• Cardiac syncope: arrhythmias or structural cardiac

diseases
10
 Vasovagal syncope

TO
• Most common form of neurally mediated syncope,

• Results from
– excessive vagal tone,
– abnormal catecholamine response to stress,
– venous pooling during an upright stance
– and impaired cardiac filling.

• The frequency of vasovagal syncopes varies

D
considerably from one to two during a lifetime to as
common as more than once a day.
11
 Mechan!sms are Important

β bylowBP
st!mulated

D
3
!!
O
1

5 O 12
 VVS - Clinical Pathophysiology
• Neurally-mediated reflex mechanism with two
components:
O
1. Cardioinhibitory (↓ HR): bradycardia, inappropriately
slow HR for the BP

p ffbothmecha!h.net
vary!ngdegrees
2. Vasodepressor (↓ BP): vasodilation, despite heart
beats normal.
• Both components are usually present

Wieling W, et al. In: Benditt D, et al. The Evaluation and Treatment of Syncope. Futura. 2003;11-22. 13
 Clinical Features of Vasovagal
Syncope
• Symptoms of orthostatic intolerance
– dizziness, lightheadedness, and fatigue,
0
• Premonitory features of autonomic activation
– diaphoresis, pallor, palpitations, nausea, hyperventilation, and yawning.
0000
• During the syncopal event, proximal and distal myoclonus (typically arrhythmic
az
and multifocal) may occur, raising the possibility of epilepsy.

• The eyes typically remain open and usually deviate upward. Pupils are usually
dilated. Roving eye movements may occur.
__

• Grunting, moaning, snorting, and stertorous breathing may be present.

• Urinary incontinence may occur. Fecal incontinence is very rare.

• Postictal confusion is also rare

Tostl!nse!are D!odes 14
 Differential Diagnosis of Syncope: Seizures vs
syncope
Observation Seizure Syncope

Onset Sudden More gradual

Duration Minutes Seconds
Jerks Frequent Rare
Headache Frequent (after) Occasional (before)
Confusion after Frequent Rare
Incontinence Frequent Rare
Eye deviation Horizontal Vertical (or none)
Tongue biting Frequent Rare
Prodrome Aura Dizziness
EEG Often abnormal Usually normal
15
 ORTHOSTATIC HYPOTENSION
• Defined As: systolic drop at least 20 mmHg or diastolic drop at least 10
mmHg within 3 min of standing
Fg
F
• Is a manifestation of sympathetic vasoconstrictor (autonomic) failure

• In most cases, there is no compensatory increase in HR despite

hypotension; 0
– with partial autonomic failure, HR may increase but insufficient to maintain CO

• “delayed” orthostatic hypotension, occurs beyond 3 min of standing;

reflects mild or early sympathetic adrenergic dysfunction.

• “initial” orthostatic hypotension occurs within 15 s of standing:

Deb
reflects a transient mismatch between CO and PVR, and does not
represent autonomic failure.

16
 ORTHOSTATIC HYPOTENSION
• Iatrogenic (drug induced)
!f
• Primary autonomic failure: idiopathic central
I
and peripheral neurodegenerative disease
üParkinson dis., Shy-Drager syndrome, Lewy0
body dementia
• Secondary autonomic failure: autonomic
peripheral neuropathies
üdiabetes, primary amiloidosis, hereditary
EE

amiloidosis, hereditary autonomic

neuropathies, immune-mediated autonomic
neuropathy
17
 Characteristic symptoms of
Orthostatic hypotension
• lightheadedness, dizziness, and presyncope

• nonspecific, such as generalized weakness, fatigue, cognitive slowing, leg buckling, or

e
headache.

• Visual blurring - due to retinal or occipital lobe ischemia.

• Neck pain, suboccipital, posterior cervical, and shoulder region (the “coat-hanger
headache”), - neck muscle ischemia

•
apices) 0
Orthostatic Dyspnea – VQ mismatch due to inadequate perfusion of ventilated lung

• Angina - impaired myocardial perfusion

• Symptoms exacerbated by exertion and prolonged standing

18
 Iatrogenic Orthostatic Hypotension
• Drugs may lower peripheral resistance
–
–
–
–
ELF
Alpha-adrenoreceptor antagonists
antihypertensive agents of several classes
nitrates and other vasodilators;
Tricyclic agents
– phenothiazines

• Iatrogenic volume depletion due to diuresis

0
• Volume depletion due to medical causes
– hemorrhage,
– vomiting,
– diarrhea,
– decreased fluid intake
19
 EVALUATION AND APPROACH
TO SYNCOPE
• The initial evaluation should answer three key
questions:

TIFF.ms
– Is it a syncopal episode or other type of
event?
– Has the etiology been determined?
– Is there evidence suggestive of a high risk of
cardiovascular events or death? 0
0
to decrease mortal!ty

20
 Syncope Mortality
• Low mortality vs.
high mortality
• Neurally-
mediated
syncope vs.
syncope with a
cardiac cause
S!m!larsurv!val

decreased
surv!val

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] 21
 A Diagnostic Plan is Essential
• Initial Examination
–Physical exam
–ECG
Go
–Detailed patient history

–Supine and upright

blood pressure
• Monitoring
işe

–Holter
–Event
–Insertable Loop Recorder (ILR)
• Cardiac Imaging (echo, MRI, CT)
• Special Investigations
–Head-up tilt test
–Hemodynamics
–Electrophysiology study
Brignole M, et al. Europace, 2004;6:467-537.
22
 Initial Exam: Detailed Patient History
t
görgü antg!
·
• Circumstances of recent event
– Eyewitness account of event

EE
– Symptoms at onset of event
– Sequelae
– Medications
• Circumstances of more
remote events
• Concomitant disease,
especially cardiac
• Pertinent family history
– Cardiac disease
– Sudden death
– Metabolic disorders
• Past medical history
– Neurological history
– Syncope
Brignole M, et al. Europace, 2004;6:467-537. 23
 Initial Exam: Thorough Physical
• Vital signs
– Heart rate
7
– Orthostatic blood pressure change
• Cardiovascular exam: Is heart disease present?
– ECG: Long QT, pre-excitation, conduction system disease
– Echo: LV function, valve status, HCM
•
E
Neurological exam
• Carotid sinus massage
– Perform under clinically appropriate conditions preferably
during head-up tilt test
– Monitor both ECG and BP

Brignole M, et al. Europace, 2004;6:467-537.

24
 Syncope
Evaluation and Differential Diagnosis
History – What to Look for

§ Complete Description
Ø From patient and observers

§ Type of Onset
§ Duration of Attacks
§ Posture
§ Associated Symptoms aura d!zz!ness
l!ghtheadedness
§ Sequelae
25
 Differential diagnosis

Temporary autonomic dysregulation of blood pressure

(seeing or
G 000 donating blood)
(heat exposure)

Acute stress, anxiety, emotional upsets

a
Situational syncope (urinating, coughing, swallowing, after a meal)

Fatigue and exhaustion (over-exertion)

26
 Differential diagnosis

Chronically impaired autonomic regulation

27
 Differential diagnosis
D

EEE

28
 12-Lead ECG

§ Normal or Abnormal?
Ø Acute MI

Ø Severe Sinus Bradycardia/pause

0
Ø AV Block

Ø Tachyarrhythmia (SVT, VT)

Ø Preexcitation (WPW), Long QT, Brugada

§ Short sampling window (approx. 12 sec)

__

29
 Carotid Sinus Massage
Fetectorofs!nshypersens!t!v!ty

§ Site:
ØCarotid arterial pulse just below thyroid cartilage
are

§ Method:
0
Ø Right followed by left, pause between önce b!r taraf
sonrabekley!p
C
Ø Massage, NOT occlusion

Ø Duration: 5-10 sec

d!ğer taraf

Ø Posture – supine & erect

30
 Carotid Sinus Massage

§ Outcome:

INGS
Ø 3 sec asystole and/or 50 mmHg fall in systolic blood
pressure with reproduction of symptoms =
Kee
Carotid Sinus Syndrome (CSS)
§ Contraindications
ETTI
Ø Carotid bruit, known significant carotid arterial disease,
previous CVA, MI last 3 months

§ Risks
Ø 1 in 5000 massages complicated by TIA
0
31
 β !f rest!ngECG !s normal we evaluate w!thth!s

Ambulatory ECG

0 0
0 0
d!sadvantage

0 00
0

32
 Ventr!cular Tachycard!a

start suddenly
Value of
Event
Recorder
in
Syncope

*Asterisk denotes
event marker Stop suddenly
Linzer M. Am J Cardiol. 1990;66:214-219.

33
 Head-up Tilt Test (HUT)
Check BP HR symptoms
§ Unmasks VVS
susceptibility
§ Reproduces symptoms

D
§ Patient learns VVS
warning symptoms
C
§ Physician is better able
to give prognostic /
treatment advice

34
 Head-Up Tilt Test (HUT)
• Protocols vary
• Useful as diagnostic
adjunct pas
60° - 80°
in atypical syncope
cases
• Useful in teaching
patients
to recognize prodromal
symptoms EE

• Not useful in assessing

treatment
Brignole M, et al. Europace. 2004;6:467-537. 35
 Vasovagal Syncope
General Treatment Measures
• Optimal treatment • Long-term prevention
strategies for VVS are – Tilt training
a source of debate – Education, instruction
• Treatment goals – Diet, fluids, salt
– Acute intervention – Support hose preventpool!ng

TEZ
• Physical maneuvers, eg, – Drug therapy note
crossing legs or tugging arms f!rstl!ne therapy
– Pacing
• Lowering head
• Lying down

Brignole M, et al. Europace, 2004;6:467-537. 36

 VVS - Pharmacologic Treatment

• Fludrocortisone
• Beta-adrenergic blockers
– Preponderance of clinical
evidence suggests minimal
benefit1
• SSRI (Selective Serotonin
Re-Uptake Inhibitor)
– 1 small controlled trial2
• Vasoconstrictors
– 1 negative controlled trial
(etilefrine)3
– 2 positive controlled trials
(midodrine)4,5
1BrignoleM, et al. Europace, 2004;6:467-537.
2Di 4Ward C, et al. Heart. 1998;79:45-49.
Girolamo E, et al. JACC. 1999;33:1227-1230. 37
3Raviele A, et al. Circ. 1999;99:1452-1457. 5Perez-Lugones A, et al. J Cardiovasc Electrophysiol. 2001;12(8):935-938.
 S!nus Bradycard!a
ECG 1

Gül
norm
Intervals

38
Supraventr!cular Tachycard!a SUT
ECG 2

39
 Th!rd Degree AV Block

ECG 3

pwaveh!d!ng
0P 0 0

reg.IE 30s

Negat!ve T wavers

or
w QRS

İLÇEKEYIF 3rd Degree AvBlock 40

Ventr!cular Tachycard!a
ECG 4

41
The end

42