SYNCOPE

BY- DR. ABDUL RAZAK

POST GRADUATE ORAL SURGERY
B.I.D.S.,BANGALORE
Definition
Syncope is defined as a sudden transient loss of
consciousness without prodromal symptoms that is followed
within seconds to minutes by resumption of consciousness,
usually with the premorbid status intact

Loss of consciousness however brief represents a potentially

life threatening situation requiring prompt recognition &
management.
Causes
Neurogenic causes
a)Breath holding
b)Vasovagal syncope
c)Vasopressor syncope
d)Orthostatic hypotension
e)Seizure disorder

Vascular causes
a)Cerebrovascular disease
b)Pulmonary embolism
c)Aortic arch syndromes

Endocrinopathies
a)Hypoglycemia
b)Addisonian crisis
c)hypothyroidism
Exposure to Toxins & Drugs

Psychogenic problems

Cardiogenic causes
a)Valvular heart disease
b)Myocardial infarction
c)Congenital heart anomalies
d)Pacemaker syndrome

Disorders of Oxygenation
a)Anemia
b)High altitude exposure
c)barotrauma
 Vasodepressor syncope
Also known as vasovagal syncope is frequently observed usually benign & self limiting
process that if not managed correctly is life threatening.
This syncope is most common type of syncope

Predisposing factors
Psychogenic factors
a)Fright
b)Anxiety
c)Emotional stress
d)Sudden & unexpected pain
e)Sight of blood or surgical or other dental instruments

Nonpsychogenic factors
a)Erect sitting or standing posture
b)Hunger from dieting or missed meal
c)Exhaustion
d)Poor physical condition
e)Hot,humid,crowded environment
f)Male gender
g)Age between 15-35 years
Prevention
It involves elimination of those factors that predispose an indiviual to
faint

Adequate air conditioning

Advice patient to have meal before dental procedure

Proper positioning of patient either supine or semisupine

Anxiety relief by psychosedation

Clinical Manifestations
Presyncope
•Early
a)Warm feeling
b)Pale or ashen-gray skin colour
c)Heavy perspiration
d)Bad feeling or feeling of faint
e)Nausea
f)Decrease in blood pressure
g)Tachycardia

•Late
a)Pupillary dilatation
b)Hyperpnea
c)Cold hands & feet
d)Hypotension
e)Bradycardia
f)Blurring of vision
g)dizziness
h)Loss of consciousness
Syncope
•Breathing become irregular, jerky & gasping
•Respiratory arrest
•Pupils dilate
•Convulsive movements & muscular twitching of hands,legs or facial muscles
•Severe bradycardia
•Severe hypotension

Postsyncope recovery
•Pallor
•Nausea
•Weakness
•Sweating
•Confusion
•Blood pressure begin to rise slowly
•Heart rate increases slowly
Pathophysiology
Patient subjected to stress
Release of high amount of catecholamines epinephrine &
norepinephrine
Pheripheral vascular dilatation
Increase blood flow to skeletal muscles
Action of the muscles returns the blood to the heart
No pheripheral pooling occurs

Patient sitting in dental chair & restricted muscle activity

Prevents return of blood
Causing pooling of blood
Thus relative decrease in circulating volume of blood, fall in arterial
blood pressure, decrease cardiac output, decrease cerebral flow
Critical level of cerebral blood flow is about 30ml per 100g of
brain tissue
Normal cerebral blood flow is 50-55ml per 100g of brain
tissue

In patient under stress with restricted muscle activity, the

cerebral blood flow decreases below critical level & results in
loss of consciousness
 Postural hypotension
Also known as orthostatic hypotension, is the second leading cause of
syncope in dental settings

Postural hypotension defined as a disorder of the autonomic nervous

system in which syncope occurs when the patient assumes an upright
position

It may also be defined as a drop in systolic pressure of 30mm Hg or

greater, or 10mm Hg or greater drop in diastolic pressure that occurs on
standing
Predisposing factors
Administration & ingestion of drugs
Prolonged recumbency & convalescence
Inadequate postural reflex
Pregnancy
Age
Venous defects in the legs
Addison’s disease
Physical exhaustion & starvation
Chronic postural hypotension
Prevention
Detailed medical history
Physical examination
•Recording of vital signs- blood pressure,heart rate, pulse, respiratory rate,
temperature
•In patient with risk of postural hypotension blood pressure should be recorded at
supine as well as in standing position
•Normal response to this reading is,
a)Systolic blood pressure 10mm Hg higher at standing position
b)Heart beats 5-20 beats faster at standing position

Clinical Criteria of Postural Hypotension

a)Standing pulse increases atleast 30 beats per minutes
b)Standing systolic blood pressure decreases atleast 25mm Hg
c)Standing diastolic blood pressure decreases atleast 10mm Hg

Dental therapy consideration

a)Slowly reposition patient upright
b)Stand nearby as patient stands
Pathophysiology
Normal regulatory mechanism
When patient changes to upright postion from supine, influence of
gravity on the cardiovascular system intensifies
Now the blood pumped from the heart must move upwards against
gravity to maintain cerbral blood flow
There is a fall in blood pressure, with systolic blood pressure
decreased by 5-40mm Hg
This is followed by rapid increase in systolic blood pressure, &
maintaining 10mm Hg higher than supine
Diastolic blood pressure also increases by 10-20mm Hg & heart rate
increase by 5-20 beats per min
Number mechanisms are involved in this
a)A reflex arteriolar constriction mediated through baroreceptors
located at carotid body & aortic arch
b)A reflex increase in heart rate
c)A reflex venous constriction that increases the venous return
d)An increase in muscle tone & contraction in the legs & abdomen,
increase venous return to heart
e)A reflex increase in respiration
f)Release of various neuorhumoral substance such as norepinephrine,
antidiuretic hormone, renin & angiotensin

Failure of one or more of the adaptive mechanism results in decrease

in blood pressure & cerebral flow below critical level
At postural hypotension,
a)Systolic blood pressure decreases by 25mm Hg or more
b)Diastolic blood pressure decreases by 10mm Hg or more
c)Heart rate increases more than 30 beats per min
 Acute Adrenal Insufficiency
Third potentially life-threatening situation that may result in the loss of
consciousness is acute adrenal insufficiency

Adrenal insufficiency is of 2 types

a)Primary adrenal insufficiency\Addison’s Disease – due deficiency of
endogenous secretion of cortisol by adrenal gland
Secondary adrenal insufficiency – produced by prolong administration
of pharmalogical doses of exogenous corticosteriods

when these patients are subjected to stress, body is unable to meet

the required concentration of corticosteroids required to adapt against
stress
This results in the peripheral vascular collapse & cardiac arrest
Pathophysiology
Normal adrenal function
•The daily secretion of corticosteroid from adrenal cortex is regulated
by adrenocorticotropic hormone ACTH, secreted by anterior pituitary
•In nonstressed situation circulatory cortisol regulates the release of
ACTH
•Under stressful situation, pituitary gland rapidly increase the release of
ACTH, which stimulates the adrenal gland to release coritisol, thus
preparing the patient to adapt to stress
•When central nervous system receives stressful stimuli, hypothalamus
receives the stimulus & releases a substance known as corticotrophine
releasing hormone CRH
•This acts on anterior pituitory to release ACTH & which in turn cause
increase in release of cortisol
Adrenal insufficiency
•Patient with primary adrenal insufficiency have hypofunctioning of
adrenal cortices, & the necessary level of cortisol required to maintain
life under nonstressful condition is supplied by exogenous
glucocorticosteroids
•In patient with normal functioning adrenal cortex, under exogenous
glucocorticosteroids theraphy, circulatory level of cortisol is maintained
by both exogenous & endogenous corticosteroids, thus inhibiting the
release of ACTH from pituitary
•With further prolong duration of glucocorticosteroids therapy adrenal
gland decrease production of endogenous cortisol & thus leading to
disuse atrophy of the gland
•These patients either primary or secondary adrenal insufficiency
exposed to stress, are not able to respond to increased level of ACTH,
thus clinical manifestation of acute insufficiency occurs
Predisposing factors
•After sudden withdrawal of steroids hormone in patient with primary
adrenal insufficiency
•After sudden withdrawal of steroids hormone is patient with secondary
adrenal insufficiency
•After stress either physiological or psycological
•After sudden destruction of pituitary gland
•After both adrenals are injured through trauma, hemorrhage or
infection
Prevention
Detailed medical history
Glucocorticosteroid coverage

Clinical manifestation
Symptoms
•Weakness, tiredness, fatigue
•Anorexia
•Vomitting
•Nausea
•Postural hypotension
•Muscle pain

Signs
•Hyperpigmentation
•Hypotension
•Hypoglycemia
•Loss of consciousness
Management
1.Assessment of consciousness
2.Termination of dental treatment
3.Position the patient
4.Assess & maintain Airway
•Head-tilt Chin-lift
•Jaw-thrust techinique

5. Assess & maintain Breathing

•Look listen & feel

6.Breathing by artificial ventilation

•Exhaled air ventilation
a)Mouth to mouth
b)Mouth to nose
•Atmospheric air ventilation
a)Bag-value mask device
b)Airway adjunct- oropharyngeal or nasopharyngeal
•Oxygen enriched ventilation
7. Assess circulation
•Carotid artery pulsation
•Chest compression

8. Definitve management
•Use of respiratory stimulant as aromatic ammonia
•Anticholinergic, atropine IV or IM
•100mg hydrocorisone IV or IM
•IV Fluids normal saline or 5%dextrose
•Hypoglycemia can be treated with 50% dextrose IV
•1-2mg of Glucagon IM
THANKING YOU