Syncope, More Than Symptom: Mohamed Abd El Zaher

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Syncope, more than

symptom
Mohamed Abd El Zaher
Lecturer of cardiology
Ain Shams University
2009
Agenda
 Definition.
 Prevalence.
 Causes and classification.
 Prognosis.
 Tests for diagnosis.
 Approach for diagnosis.
 Management.
Agenda
 Definition.
 Prevalence.
 Causes and classification.
 Prognosis.
 Tests for diagnosis.
 Approach for diagnosis.
 Management.
Defintion
 Sudden, Transient, loss of consciousness and
postural tone with spontaneous recovery.

(Due to cerebral hypoperfusion and not requiring


electrical or chemical therapy for reversal)
(Restoration of appropriate behavior and
orientation after a syncopal episode is usually
immediate)
The metabolism of the
brain is exclusively
dependent on perfusion.

Consequently, cessation
of cerebral blood flow
leads to loss of
consciousness within
approximately 10
seconds
Syncope excludes seizures, coma, shock, or
other states of altered consciousness.
Agenda
 Definition.
 Prevalence.
 Causes and classification.
 Prognosis.
 Tests for diagnosis.
 Approach for diagnosis.
 Management.
:Prevalence
Syncope is an important clinical
problem because it is
 Common.
 Costly.
 Often disabling.
 may cause injury.
 and may be the only warning sign before
sudden cardiac death. (HCM, long QT,
Brugada, ARVD)
Syncope account for 1 % of hospital admissions
and 3 % of emergency department visits.
Age related prevalence

 In young individuals, NMS is the most


common.

 syncope in elderly include orthostatic


hypotension, medication, aortic stenosis,
carotid sinus hypersensitivity, and
bradyarrhythmias.
Agenda
 Definition.
 Prevalence.
 Causes and classification.
 Prognosis.
 Tests for diagnosis.
 Approach for diagnosis.
 Management.
Classification of syncope
True Syncope

(cerebral hypoperfusion)
 Vascular (Neurally
mediated , sitiuational &
orthostatic).
 Cardiac
(arrhythmias,
anatomical)
Classification of syncope
True Syncope Condition mimic
syncope
(cerebral hypoperfusion) (no cerebral hypoperfusion)
 Vascular (Neurally  Neurologic disease
mediated , sitiuational & (Epilepsy, TIA).
orthostatic).  Metabolic
 Cardiac (Hypoglycemia, hypoxia
(arrhythmias, and alcohol)
anatomical)  Psychogenic (Anxiety,
panic, conversion reaction).
 Vascular causes of syncope are most common,
followed by cardiac causes. (True syncope)

 Among cardiac causes of syncope,


arrhythmias are most common.

 Neurological causes of apparent syncope are


surprisingly uncommon, accounting for less
than 10 % of all cases of syncope.
Vascular causes for syncope
I- Orthostatic Hypotension :
Definition: 20-mmHg drop in systolic blood
pressure or a 10-mmHg drop in diastolic
blood pressure within 3 minutes of standing.
Precipitating factors:
Volume depletion.
Vasodilators.
Elderly (↓ baroreceptor sensitivity, ↓ cerebral
blood flow, renal sodium wasting, and an
impaired thirst mechanism with aging ).
Mechanism

800 ml of blood is displaced to the


abdomen and lower extremities

↓ cop abrupt drop of the VR

stimulation of aortic & carotid, baroreceptors

Increase in sympathetic outflow ( VC and ↑ HR)


:Causes of failure of this mechanism

 Drugs:

Diuretics.
VD.
Alcohol
:Causes of failure of this mechanism

 Drugs:  Autonomic failure:


1. Primary:
Diuretics.  Pure autonomic failure.
VD.
 Multisystem atrophy
(shy-dragger S).
Alcohol 2. Secondary:
 Aging.
 CNS (MS-tumor).
 Medical (DM-CRF).
 Autoimmune (SLE,
RHD).
II- Reflex mediated syncope
Trigger= Response=
afferent efferent limb
limb Vagal ++.
 Prolonged Symp –
standing
 Carotid ++.
 Micturation. Bradycardia, ↓Bpr
 Syncope
II- Reflex mediated syncope
Trigger= Response=
afferent efferent limb
limb Vagal ++.
 Prolonged Symp –
standing
 Carotid ++.
 Micturation. Bradycardia, ↓Bpr
 Syncope
Fixed
Variable
A) Neurally mediated syncope:
= neurocardiogenic, vasovagal:
Trigger: Prolonged standing. Hot weather.
Sight of blood. Pain.
Response: Vasodepressor - cardioinhibitory or
mixed.
Mechanism: trigger ↓VR ↓CO ++BR

++Vagal of mechano. r ++ ++ Symp


B) Carotid Sinus Hypersensitivity:
Trigger:  Carotid stimulation.
Response: the same.
Mechanism: ++ of carotid sinus baroreceptors.
Carotid sinus massage:
 In both the supine and upright positions.

 Gentle pressure over the carotid pulsation.

 5 to 10 seconds.

 Avoided if (bruits, recent CVS or TIA). CVS.


For positive test:
 Pause > 3 seconds.

 >50 mmHg drop in sys Bp.

 >30 mmHg drop in sys Bp with symptoms.


Cardiac causes for syncope
Anatomical Arrhythmias
 MS-AS.  Brady.

 HoCM.  Tachy.

 Tamponade.

 MI.

 Ao. Dissection.

 PE.
Agenda
 Definition.
 Prevalence.
 Causes and classification.
 Prognosis.
 Tests for diagnosis.
 Approach for diagnosis.
 Management.
Prognosis
 Varies greatly with the diagnosis.

 Syncope of unknown origin or syncope with a


noncardiac cause (including reflex-mediated
syncope) is generally associated with a benign
prognosis.

 Syncope with a cardiac cause is associated


with up to 30 percent mortality at 1 year.
Evaluation and diagnosis
I- History:
 Most imp.
 Can identify up to 25% of cases.

 You can ask about:

 Syncope or mimic.  ppt factors.


 Cardiac ds.  F Hx.
 Prior attacks.
:II- Physical examination
.Bp. (supine & standing) *
.Cardiac examination *
.Neurological examination *
:III- ECG
.Clue for cardiac disease
.Diagnosis of arrhythmias
Normal ECG linked with better prognosis
IV- Blood tests:
(serum electrolyte, cardiac enzyme, glucose,
and hematocrit levels, are of low diagnostic
value.
As a result, the routine use of laboratory tests
is not recommended for patients with
syncope.
V- Continuous ECG recording:
A- Holter:
Suspected arrhthymias.
Recurrent syncope.
B- Loop recorder:
Infrequent episode.
Other causes excluded.
C- Implantable event recorder:
After full evaluation with –ve results.
VI- Echocardiography:
Not routine.
If organic ht disease is suspected.

VII- Upright tilt-table testing:


• Gold standard for Neurally mediated syncope.

VIII- Ex ECG:
* Syncope occurred during or immediately
after exertion .
IX- EPS:
• Arrhythmia suspected but not confirmed.

• Differentiate between different arrhythmias.

• High risk occupation ???.

X- Neurological tests:
• EEG, CT, MRI, carotid duplex.

• rarely diagnostic, overused.

• Consider vertebrobasilar insufficiency.


Agenda
 Definition.
 Prevalence.
 Causes and classification.
 Prognosis.
 Tests for diagnosis.
 Approach for diagnosis.
 Management.
Approach to the Evaluation of
Patients with Syncope
Agenda
 Definition.
 Prevalence.
 Causes and classification.
 Prognosis.
 Tests for diagnosis.
 Approach for diagnosis.
 Management.
Management
1- Treatment of the cause, <the most imp>.
 HCM….
 IHD…
 PE.
 Tamponade.
 Brady…..
 Tachy…
 ARVD, Long QT, Brugada……
?Should I hospitalize

Yes, if:
1. Suspect heart disease.
2. Abnormal ECG.
3. Severe injury.
4. F hx of SCD.
5. Syncope with exertion.
What about neurally mediated
?????syncope
1. Reassurance.
2. Avoid PPT factors.
3. During syncope: lie down, elevate the leg.
4. In between attacks:
 ↑ Na++ in diet.
 Avoid dehydration.
 Physical measures is well accepted option,
isometric hand grip, standing wall (40 min. twice
daily).
 Drugs: (BB, midodrine and fludrocortisone).
 PPM only if (>5 episodes/yr, severe physical
injury and age>40 yrs.
Thank You
Thank You

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