DR. RAJESH T EAPENSPECIALIST – ANESTHESIA ATLAS HOSPITAL RUWI
What is Syncope?• Common clinical problem and a primary goal of evaluation is to determine whether the patient is at increased risk of death.
Definition• Sudden, self-limited loss of consciousness in postural tone caused by transient global cerebral hypoperfusion & followed by spontaneous complete and prompt recovery
History• It is vital to establish exactly what patients mean by blackout• Do they mean loss of consciousness (LOC)?• A fall to the ground without loss of conscious-ness?• A clouding of vision, diplopia, or vertigo?• Take a detailed history from the patient and a witness
Epidemiology• Common in the general population - 6% of medical admissions - 3% of Emergency room visits• Incidence: Male = Female
Risk Factors• Cardiovascular disease, h/o stroke or TIA & HTN• Low BMI, ↑alcohol intake & diabetes or elevated blood glucose concentration
Vasovagal (neuro-cardiogenic)syncope• Due to reflex bradycardia ± peripheral vasodilatation provoked by emotion, pain, fear or standing too long• Onset is over seconds (not instantaneous), and is often preceded by nausea, pallor, sweating and closing in of visual fields (pre-syncope)• It cannot occur if lying down
Vasovagal (neuro-cardiogenic)syncope …..contd.• The patient falls to the ground, being unconscious for ~2 min• Brief clonic jerking of the limbs may occur (reflex anoxic convulsion due to cerebral hypo-perfusion), but there is no stiffening or tonic → clonic sequence• Urinary incontinence is uncommon (but can occur), and there is no tongue-biting.• Post-ictal recovery is rapid
Situation syncope• Syncopal symptoms are as described for vasovagal syncope• Cough syncope: Syncope after a paroxysm of coughing• Effort syncope: Syncope on exercise; cardiac origin, e.g. aortic stenosis, HOCM• Micturition syncope: Syncope during or after micturition. Mostly men, at night• Even during swallowing & defecation!
Carotid sinus syncope• Hypersensitive baroreceptors cause excessive reflex brady-cardia ± vasodilatation on minimal stimulation (e.g. head-turning, shaving)
Epilepsy• Attacks vary with the type of seizure,• Certain features are more suggestive of epilepsy: attacks when asleep or lying down aura identifiable triggers. e.g. TV altered breathing cyanosis typical tonic-clonic movements incontinence of urine tongue-biting (ask about a sore tongue after the fit) prolonged post-ictal drowsiness, confusion, amnesia and transient focal paralysis (Todds palsy)
Stokes-Adams attacks• Transient arrhythmias (e.g. bradycardia due to complete heart block) causing ↓ cardiac output and LOC• The patient falls to the ground (often with no warning except palpitations), pale, with a slow or absent pulse• Recovery is in seconds, the patient flushes, the pulse speeds up, and consciousness is regained
Stokes-Adams attacks …contd.• Injury is typical of these intermittent arrhythmias• As with vasovagal syncope, a few clonic jerks may occur if an attack is prolonged, due to cerebral hvpo- perfusion (reflex anoxic convulsion).• Attacks may happen several times a day and in any posture
Drop attacks• Sudden weakness of the legs causes the patient, usually an older woman, to fall to the ground• There is no warning, no LOC and no confusion after-wards• The condition is benign, resolving spontaneously after a number of attacks.• Other causes: hydrocephalus (these patients, however. may not be able to get up for hours); cataplexy-triggered by emotion (associated with narcolepsy)
Other causes• Hypoglycaemia: Tremor, hunger, and perspiration herald light-headedness or LOC; rare in non-diabetics• Orthostatic hypotension: Unsteadiness or LOC on standing from lying in those with inadequate vasomotor reflexes: the elderly; autonomic neuropathy; antihypertensive medication; over-diuresis; multi-system atrophy (MSA)• Anxiety: Hyperventilation. tremor, sweating. tachycardia, paraesthesias, light-headedness, and no LOC suggest a panic attack.
Other causes ……….contd.• Factitious blackouts: pseudo-seizures, Munchausens• Choking: If a large piece of food blocks the larynx, the patient may collapse, become cyanotic, and be unable to speak. Do the Heimlich manoeuvre immediately to eject the food
Examination• Cardiovascular• Neurological• BP lying and standing
Investigations• ECG ± 24h ECG (arrhythmia, long QT, e.g. Romano- Ward)• U&E, FBC. glucose• Tilt-table tests• EEG, sleep EEG• Echocardiogram• CT/MRI brain• HUT (Head Up Tilt test)• PaCO2 ↓ in attacks suggest hyperventilation as the cause• While the cause is being elucidated, advise against driving
Treatment – Neurocardiogenic Syncope • Counsel patients to take precautionary steps to avoid injury by being aware of prodromal symptoms & maintaining a horizontal position at those times • Avoid known precipitants & maintain adequate hydration • Employ isometric muscle contractions during prodrome to abort episode • Midodrine (start at 5mg PO Tid & can be increased to 15mg Tid) probably helpful in the treatment • Cardiac pacing for carotid sinus hypersensitivity is appropriate in syncopal patients
Treatment – Orthostatic hypotension • Adequate hydration & elimination of offending drugs • Salt supplementation, compressive stocking & counselling on standing slowly • Midodrine & fludrocortisone can help by increasing systolic BP & expanding plasma volume respectively
Treatment – Cardiovascular (arrhythmia ormechanical): • Treatment of underlying cause(valve replacement, antiarrhythmic agent, coronary re-vascularisation etc.) • Cardiac pacing for sinus node dysfunction or high- degree AV block • Discontinuation of QT prolonging drugs • Catheter ablation procedure in select patients with syncope associated with SVT • ICD for documented VT without correctable cause and for syncope with EF < 35% even in absence of documented arrhythmia