Assessment and Management of Syncope

1. SYNCOPE
By,
Sreelekshmi J
Intern
KVG Dental College

2. CONTENTS
• Definition
• Classification
• Predisposing factors
• Prevention
• Dental Consideration
• Clinical manifestations
• Pathophysiology
• Investigations
• Management
• References

3. DEFINITION
• Syncope is defined as sudden and transient loss
of consciousness which is secondary to period of
cerebral ischemia.
• The term “syncope” is
derived from the Greek word
which means “to cut short”
or “interrupt.”

4. • Syncope and faintness occurs in upright posture
except ‘Stokes-Adams’ attack in which syncope
occurs in sitting and standing position.
• A syncopal prodrome (presyncope) is common,
although loss of consciousness may occur
without any warning symptoms.
• Typical presyncopal symptoms include dizziness,
lightheadedness or faintness, weakness, fatigue
and visual and auditory disturbances.

5. CLASSIFICATION
1. Neurally mediated reflex syncope
• Vasovagal syncope
• Carotid sinus syndrome
• Situational faints (e.g., cough, defecation,
excessive heat, micturition, pain, prolonged
upright posture, sneeze, swallow, venipuncture,
volume depletion)
• Other (e.g., weightlifting, post-prandial)

6. 2. Orthostatic syncope
• Secondary autonomic failure syndromes (e.g.,
diabetic neuropathy, amyloid neuropathy, drugs
and alcohol)
• Volume depletion (e.g., hemorrhage, diarrhea,
Addison’s disease)
• Primary autonomic failure syndromes (e.g., pure
autonomic failure, multiple system atrophy,
Parkinson’s disease with autonomic failure)
• Postural intolerance syndromes (e.g., postural
orthostatic tachycardia syndrome) in which
syncope occurs occasionally, probably of reflex
origin

7. 3. Cardiac arrhythmias as primary cause
• Implanted device (pacemaker) malfunction
4. Structural cardiac or cardiopulmonary disease
• Acute myocardial infarction/ischemia
• Cardiac valvular disease
• Pulmonary embolus/pulmonary hypertension
• Pericardial disease/tamponade
5. Cerebrovascular

8. PREDISPOSING FACTORS
• In the dental setting, stress is the primary cause
in most cases of unconsciousness. The sudden
loss of consciousness (syncope) that occurs
during venipuncture or the intraoral injection of a
local anesthetic is a classic example of
vasodepressor syncope.

9. • Impaired physical status is another factor
working to increase the likelihood of syncope.
When patients with impaired physical status
are exposed to undue stress, whether
physiologic or psychological, the chances are
even greater that they may react adversely to
the situation. For example, persons with
underlying cardiovascular disease may
respond with sudden cardiac arrest secondary
to acute cardiac dysrhythmias, which are
precipitated by the same physiologic stress
that may cause vasodepressor syncope in a
healthy individual.

10. • A third factor associated with loss of
consciousness is the administration or ingestion
of drugs. The three major categories of drugs
used in dentistry are analgesics (nonopioids,
including nonsteroidal antiinflammatory drugs;
opioid analgesics; and local anesthetics),
antianxiety agents (anxiolytics and sedative-
hypnotics), and antibiotics.

11. • Drugs in the first two categories are CNS
depressants and therefore produce alterations in
the level of consciousness (e.g., sedation) or the
loss of consciousness. Some of these drugs,
primarily the opioid agonists, predispose the
ambulatory dental patient to orthostatic (postural)
hypotension. Opioids and other CNS-depressant
drugs, if administered in larger doses, can induce
the loss of consciousness as the CNS is
progressively depressed to the point at which
consciousness is lost.

12. PREDISPOSING FACTORS FOR
VASOVAGAL SYNCOPE
PSYCHOGENIC FACTORS NONPSYCHOGENIC
FACTORS
Fright
Anxiety
Emotional stress
Receipt of unwelcome news
Pain, especially sudden and
unexpected
Sight of blood or surgical or other
dental instruments (e.g., local
anesthetic syringe)
Erect sitting or standing posture
Hunger from dieting or a missed
meal
Exhaustion
Poor physical condition
Hot, humid, crowded environment
Male gender(Age between 16 and
35 years)

13. PREDISPOSING FACTORS FOR
POSTURAL HYPOTENSION
1) Drug administration and ingestion
• Antihypertensives especially sodium-depleting
diuretics, calcium channel blockers.
• Sedatives and tranquilizers
• Antiparkinsonism drugs like levodopa.
• Phenothiazines like chlorpromazine, thioridazine.
Positional changes should be made slowly and
carefully in patients receiving these drugs

14. 2) Prolonged recumbency and convalescence
• Patients may remain recumbent in the dental
chair for treatment lasting as long as 2 or 3 hours.
• In these circumstances, postural hypotension
may develop when the dental chair is returned
quickly to the upright position or the patient
stands.

15. 3) Inadequate postural reflex
• Healthy young people may faint when forced to
stand motionless for prolonged periods, such as
during school assemblies, religious services, or
parades.
• Syncope also can develop when a patient is
seated upright in the dental chair for a prolonged
period. This situation is more likely to occur in a
hot and humid environment, which produces
concomitant peripheral vasodilation.

16. 4) Pregnancy
• Supine hypotensive syndrome of pregnancy occurs
late in the third trimester if the woman remains in the
supine position for more than 3 to 7 minutes.
5) Age
• The incidence of postural hypotension shows a very
definite increase with increasing age and proves to
be a major problem in the aged population.
6) Chronic postural hypotension (Shy-Drager
syndrome)

17. 7) Venous defects in the legs
• Postural hypotension also occurs in patients with
varicose veins and other vascular disorders of the
legs. These disorders permit excessive pooling of
blood in these patients’ legs.
8) Addison’s disease
• Postural hypotension frequently occurs in patients
with chronic adrenocortical insufficiency. The
doctor may manage this condition through the
administration of corticosteroids.

18. PREVENTION
• Prevention of vasodepressor syncope is directed at
eliminating factors that predispose an individual to
faint.
• Adequate air conditioning in the dental office
eliminates the heat factor.
• Patient hunger, a result of dieting or a missed meal
before the dental appointment, also should be
considered. All patients, but especially those who are
anxious, should be requested to eat a light snack or
meal before their dental appointment to minimize the
risk of developing hypoglycemia in addition to a
psychogenic response.

19. 1) Positioning:
• The risk of vasodepressor syncope is greatly
increased in an apprehensive patient who is
either standing or seated upright during
treatment.
• Today, patients will be placed in a supine or
semisupine (30- to 45-degree) position, a practice
that has minimized the occurrence of
vasodepressor syncope during dental treatment.

20. 2) Anxiety Relief
• Each potential patient must be recognised and
evaluated for the presence of dental anxiety. If
the patient is overly anxious, dental treatment
should be modified to minimize or to eliminate it.
• The inclusion of written anxiety questionnaire in
the medical history questionnaire is worthwhile.

21. DENTAL CONSIDERATION
Follow anxiety reduction protocol.
• Premedicate the patient with hypnotics for a
relaxed sleep the night before the surgery.
• Premedicate the patient with sedatives on the day
of surgery.
• Schedule the surgery in the morning.
• Minimise the patient waiting time.
• Consider psychosedation during surgery.

22. • Administer adequate pain control measures
during surgery.
• Reduce the length of the appointment.
• Avoid any anxiety during surgery.
• Follow-up postoperative pain and anxiety control.
• Effective postoperative analgesics.

23. CLINICAL MANIFESTATIONS
• The clinical manifestations
of vasodepressor syncope
can be grouped into
3 definite phases:
i. Presyncope
ii. Syncope
iii. Postsyncope(recovery period)

24. Presyncope
EARLY SYMPTOMS LATE SYMPTOMS
• Feeling of warmth
• Loss of color; pale or ashen-
gray skin tone
• Heavy perspiration
(diaphoresis)
• Reports of “feeling bad” or
“feeling faint”
• Nausea
• Blood pressure at baseline
level or slightly lower
• Tachycardia
• Pupillary dilation
• Yawning
• Hyperpnea
• Cold hands and feet
• Hypotension
• Bradycardia
• Visual disturbances
• Dizziness
• Loss of consciousness

25. Syncope
• Breathing may
a. become irregular, jerky, and gasping;
b. become quiet, shallow, and scarcely
perceptible; or
c. cease entirely (respiratory arrest or apnea).
• The pupils dilate, and the patient takes on a
deathlike appearance.
• Bradycardia, which develops at the end of the
presyncopal phase, continues.
• Decreased blood pressure.

26. • The pulse becomes weak and thready.
• Convulsive movements and muscular twitching of
the hands, legs, or facial muscles are common
when patients lose consciousness and become
hypoxic (a result of cerebral hypoxia/anoxia),
even for periods as short as 10 seconds.

27. Postsyncope
• In the postsyncopal phase the patient may
demonstrate pallor, nausea, weakness, and
sweating, all of which can last from a few minutes
to several hours. Occasionally, symptoms persist
for 24 hours.
• During the immediate postsyncopal phase, the
patient may experience a short period of
confusion or disorientation.

28. • The heart rate, which is depressed, also returns
slowly toward the baseline level, and the pulse
becomes stronger.
• In addition, a point worth stressing is that once a
patient loses consciousness, the tendency for
that patient to faint again may persist for many
hours if the patient assumes a sitting position or
stands too soon or quickly.

29. PATHOPHYSIOLOGY
Mechanism Clinical example
Inadequate delivery of blood or O2 to
the brain
Acute adrenal insufficiency
Hypotension
Orthostatic hypotension
Vasodepressor syncope
Systemic or local metabolic
deficiencies
Acute allergic reaction
Drug ingestion and administration
Nitrites and nitrates
Diuretics
Sedatives, opioids
Local anaesthetics
Direct or reflex effects on nervous
system
Cerebrovascular accident
Convulsive episodes
Psychic mechanisms Emotional disturbances
Hyperventilation
Vasodepressor syncope
In his classic test on fainting, Engle divided the mechanisms that
produce syncope into four categories:

30. PATHOPHYSIOLOGY OF
VASOVAGAL SYNCOPE
Anxiety
Increased release of Catecholamines
Decreased Peripheral Vascular Resistance
Pooling of Blood in the peripheries and fall in arterial blood
pressure
Compensatory mechanisms

31. Increased heart rate, rapid breathing, pallor & perspiration
Decompensation
Hypotension, Reduced cerebral blood flow
Syncope

32. INVESTIGATIONS
• Echocardiography is likely the most useful test to help risk
stratify patients as it can identify those that have structural
heart disease including valvular abnormalities, wall motion
abnormalities and pericardial effusions.
• Hematologic studies or advanced imaging, including
computed tomography scans, can be ordered based on
the history and exam.
• Electrolytes and hematocrit can be assessed in a patient
with a history of diarrhoea and vomiting or gastrointestinal
hemorrhage respectively.
• Tilt table testing in unexplained syncope in high-risk
settings or with recurrent faints in the absence of heart
disease.

33. San Francisco Syncope Rule
• CHESS
C – Congestive Heart Failure history
H – Hematocrit < 30%
E – ECG (Abnormal)
S – Shortness of breath
S – Systolic Blood pressure<90mm of Hg.
• Patients that meet any of these 5 criteria are predicted to
be at higher risk for adverse outcomes at 7 or 30 days.
• Adverse outcomes include death, myocardial infarction,
arrhythmia, pulmonary embolism, stroke, subarachnoid
hemorrhage, or significant hemorrhage.

34. MANAGEMENT
• The main aim of treatment of syncope is to avoid
fall or injury during an attack.
• Includes management of 4 separate stages of
syncope:
1) presyncope,
2) syncope,
3) delayed recovery, and
4) post-syncope.

35. Presyncope
• STEP-1(POSITION):
-As soon as presyncopal signs and symptoms are
noted, the dental procedure is terminated and the
patient placed into the supine position with legs slightly
elevated.
-This position change usually halts the progression of
symptoms.
-Muscle movement also helps increase the return of
blood from the periphery.
-If patients can move their legs vigorously, they are
less likely to experience significant peripheral pooling
of blood, minimizing the severity of the reaction.

36. • STEP-2: C  A  B
-CIRCULATION  AIRWAY  BREATHING
-Because the victim is still conscious in the
presyncopal period and can speak, C, A and B are
assessed as being adequate.
• STEP-3: D(DEFINITIVE CARE):
-O2 may be administered through use of a full-face
mask, or an ammonia ampule may be crushed
under the patient’s nose to help speed recovery

37. An aromatic ammonia vaporole is crushed between the rescuer’s
fingers and held near the patient’s nose to stimulate movement.

38. Syncope
• Basic management recommended for all
unconscious patients: P → C → A → B.
• Step 1: Assessment of consciousness.
-The patient (victim) suffering vasodepressor
syncope demonstrates a lack of response to
sensory stimulation.
• Step 2: Activation of the dental office emergency
system.
-Office team members should perform their
assigned duties.

39. • Step 3: Position
-The first and most important step in the
management of syncope is the placement of the
victim into the supine position.
-A slight elevation of the legs helps increase the
return of blood from the periphery.
-Failure to place the victim in the supine position
may result in death or permanent neurologic
damage secondary to prolonged cerebral ischemia

40. • Placement of unconscious patient in the supine position
with feet elevated slightly.

41. • Step 4: C → A → B (basic life support, as
needed).
-The victim must be assessed immediately and a
patent airway ensured.
-In most instances of vasodepressor syncope, the
head tilt–chin lift procedure successfully
establishes a patent airway.
-To assess circulation, the carotid pulse is
palpated.

42. Airway patency may be obtained through use of the head tilt–
chin lift method.

43. • Step 5: D (DEFINITIVE CARE).
i. Administration of O2. - O2 may be administered
to the syncopal or postsyncopal patient at any
time during the episode.
ii. Monitoring of vital signs. - Vital signs, including
blood pressure, heart rate, and respiratory rate,
should be monitored.

44. iii. Additional procedures.
- Loosening of binding clothes such as ties, collars
and belts.
- Use of a respiratory stimulant, such as aromatic
ammonia.
- If bradycardia persists, an anticholinergic, such
as atropine, may be considered for administration
either intravenously or intramuscularly.
- Administration of “sugar” in the form of orange
juice or a nondiet soft drink may be beneficial in
case of hypoglycemia.

45. Delayed Recovery
• If the victim does not regain consciousness after
the previous steps have been performed or does
not recover completely in 15 to 20 minutes, a
different cause for the syncopal episode should
be considered and the emergency medical
services (EMS) system activated.
• Possible causes of delayed recovery from
syncope include: seizure, cerebrovascular
accident (stroke), transient ischemic attacks
(TIA), cardiac dysrhythmias, and hypoglycemia.

46. Postsyncope
• After recovery, patients should not undergo additional
dental treatment the remainder of that day.
• Body may require up to 24 hours to return to its
normal state.
• Prior to dismissal of the patient from the dental office,
the doctor should determine the primary precipitating
event and any other factors (e.g., hunger or fear) that
might have contributed to it.
• Arrangements must be made for a responsible adult
escort(e.g., family member) to take the patient home.

47. REFERENCES
• Medical Emergencies in the Dental Office –
Stanley F. Malamed
• Textbook of Oral & Maxillofacial Surgery –
S M Balaji
• Internet