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SYNCOPE

PG OMFS, MBDC

December 12 2011

Dr. Praveen Mathew

CONTENTS Introduction Classification Vasodepressor syncope Cardiogenic syncope Neurocardiogenic syncope Situational syncope Carotid sinus hypersensitivity Postural hypotension Management

SYNCOPE Introduction Syncope refers to sudden loss of consciousness due to reduced cerebral perfusion. Presyncope refers to light headedness where the individual thinks he/she may blackout. Affects about 20% of the population at some time & accounts for more than 5% of hospital admissions. Classification

Vasodepressor syncope Is a frequently observed, usually benign & self limiting process that if not managed correctly is life threatening.

Cardiogenic syncope Caused by a sudden decline in cardiac output may be provoked by exertion in patients with severe aortic stenosis or may occur without warning in patients with cardiac arrhythmia. Synonyms Benign faint Neurogenic syncope Psychogenic syncope Simple faint Swoon Vasodepressor syncope Vasovagal syncope Predisposing factors Psychogenic factors Fright Anxiety Emotional stress Reciept of unwelcome news Pain, especially sudden & unexpected Sight of blood or surgical & other dental instruments Non psychogenic factors Erect sitting/standing posture Hunger from dieting or a missed meal Exhaustion Poor physical condition Hot, humid, crowded environment Age b/w 15 35 yrs

Features Cardiac syncope Premonitory symptoms Often none Lightheadedness Palpitation Chest pain Breathlessness Unconscious period Extreme death like pallor Recovery Rapid recovery < 1 min Flushing Neuro - cardiogenic syncope Premonitory symptoms Nausea Lightheadedness Sweating Unconscious period Pallor Recovery Slow Nausea Lightheadedness

Pathophysiology Vasodepressor syncope is most commonly precipitated by a decrease in cerebral blood flow below a critical level & usually characterized by sudden drop in BP & heart rate. Stress causes increased release of catecholamine into circulatory system. This result in changes in tissue blood perfusion & decrease in peripheral vascular resistance & increased blood flow to many tissues especially skeletal muscles. When muscular activity occurs this diverted blood volume return to heart by pumping action of muscles. In situations where muscular activity does not occur there is significant peripheral pooling of blood resulting in decreased cerebral blood flow. Compensatory mechanisms are activated to maintain adequate cerebral blood flow. Baroreceptors refluxely constrict peripheral blood vessels increasing the return of venous blood to heart. Carotid & aortic arch reflux which increase heart rate. If situation goes unmanaged, these compensatory mechanisms fatigue, which is manifested as reflux bradycardia. Slowing of heart rate < 50 beats/min is common & leads to significant drop in cardiac output which is associated with a precipitous fall in BP below critical level for maintenance of consciousness. Cerebral ischemia results & the individual lose consciousness. Differential diagnosis History taking is the key to establishing a diagnosis. Attention should be given to potential triggers, the victim s appearance, and the duration of episode & speed of recovery. Cardiac syncope is usually sudden, but can be associated with premonitory lightheadedness, palpitation or chest discomfort. Blackout is usually brief & recovery rapid.

Neurocardiogenic syncope will often be associated with a situational trigger, & patient may experience flushing, nausea & malaise for several minutes afterwards. Patients with seizures do not exhibit palour, may have abnormal movements, usually take more than 5 minutes to recover & are often confused. A history of rotational vertigo is suggestive of a labyrinthine or vestibular disorder. Arrhythmia Lightheadedness may occur with many arrhythmias but blackouts are usually due to profound bradycardia or malignant ventricular tachyarrhythmia. Key to establishing a diagnosis is to obtain an ECG recording during symptoms. Structural heart disease Severe aortic stenosis, hypertrophic obstructive cardiomyopathy & severe coronary artery disease can cause syncope on exertion. Exertional arrhythmias also occur in these patients. Neurocardiogenic syncope This includes Situational syncope Vasovagal syncope Carotid sinus syncope & Postural hypotension Situational syncope This is the collective name of neuro cardiogenic syncope that occurs in presence of identifiable triggers. i.e.

Cough syncope Micturation syncope Vasovagal syncope This is normally triggered by a reduction in venous return due to prolonged standing, excessive heat or a large meal. It is mediated by the Bezold Jarisch reflex, in which there is an initial sympathetic activation that leads to vigorous contraction of relatively under filled ventricles. This stimulates ventricular mechanoreceptors, producing para sympathetic activation & sympathetic withdrawal, causing bradycardia, vasodilatation or both. Carotid sinus hypersensitivity This causes pre syncope/syncope because of reflex bradycrdia & vasodilatation. Carotid baroreceptors are involved in BP regulation & are activated by increased BP, resulting in a vagal discharge that causes a compensatory drop in BP. Postural hypotension This is caused by failure of normal compensatory mechanism. Relative hypovolaemia (often due to excessive diuretic therapy) sympathetic degeneration (diabetes mellitus, Parkinson s disease, ageing) & drug therapy (vasodilators, antidepressants) can all cause or aggravate the problem. Treatment is often ineffective. Fludrocortisones which can expand blood volume through sodium & water retention may help. Prevention Proper positioning Anxiety relief

Management Management of syncopal patients differs depending on the signs & symptoms the individual exhibits. Presyncope 1. P (Position): As soon as the presyncopal signs & symptoms appear, the procedure should be halted & patient placed into supine position with legs slightly elevated. Muscle movement also helps increase return of blood from periphery. 2. A  B  C (airway breathing circulation): The victim must be assessed immediately & a patent airway ensured. In most instances of vasodepressor syncope, the head tilt chin lift procedure successfully establishes a patent airway. Oxygen may be administered through use of a full face mask or an ammonia ampoule may be crushed under patient s nose to speed recovery. 3. D - (definitive care): Following management of presyncope, attempts should be made to determine the cause of the episode while the patient recovers. Modifications in future dental treatment should be considered to minimize the risk of recurrence. The planned dental treatment may proceed only if both the doctor & patient feel it appropriate. Syncope Proper management of vasodepressor syncope follows the basic management recommended for all unconscious patients PABC.

Assessment of consciousness: The patient suffering vasodepressor syncope demonstrates a lack of response to sensory stimulation. Activation of dental office emergency system. P Placement of the victim in supine position: A slight elevation of legs helps increase the return of blood from the periphery. This step is so vital because of overwhelming majority of the observed clinical manifestations during syncope are the result of inadequate cerebral blood flow. Failure to place the victim in the supine position may result in death or permanent neurologic damage secondary to prolonged cerebral ischemia. This damage can occur in as little as 2 3 mins if the victim maintains an upright position. 4. ABC (basic life support): The victim must be assessed immediately & a patent airway ensured. In most instances of vasodepressor syncope, the head tilt chin lift procedure successfully establishes a patent airway. Assessment of airway patency & adequacy of breathing constitute the next actions. An adequate airway is present when the patient s chest move & exhaled air can be heard & felt. Spontaneous respiration usually is evident during syncope; however artificial ventilation may be necessary if spontaneous breathing stops. Positioning of the victim & establishment of a patent airway usually lead to return of consciousness. To assess circulation the carotid pulse must be palpated. Though rare brief periods of ventricular asystole can develop during syncope. In most circumstances a weak thready pulse is palpable in neck. Heart rate is commonly low.

5. D definitive care: 5a Administration of oxygen: Oxygen may be administered to syncopal or post syncopal patient at any time during episode. 5b Monitoring of vital signs: Vital signs, including BP, heart rate, & respiratory rate should be monitored, recorded & compared to patients pre operative baseline values to determine the severity of the reaction & the degree of recovery. 5c Additional procedures: This procedure includes the loosening of tight clothes & use of respiratory stimulant like aromatic ammonia. If bradycardia persists an anticholinergic such as atropine may be administered IV/IM. As the victim regains consciousness it is important that the doctor & emergency team maintain their composure. Stimulus that precipitated the episode must be removed from patient s field of vision. Delayed recovery If the victim does not regain consciousness in 15 20 minutes a different cause for the syncopal episode should be considered & EMS activated. If another cause of unconsciousness (hypoglycemia) becomes obvious, the doctor may initiate definitive management. In the absence of an obvious cause, however the doctor should continue BLS & if possible start an IV infusion. Post syncope After recovery from a period of syncope patients should not undergo additional dental treatment that day. Possibility of a second syncopal episode is greater during post syncopal phase. Prior to dismissal of patient, the doctor should determine the primary precipitating event & any other factors that have

contributed to it. Arrangement must be made to assist the patient safely home. To conclude Proper history & evaluation of patient can prevent dental emergencies to a certain extent.

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