Syncope ppt
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Approach to a Patient with Syncope
-Dr. Sachin Adukia
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Syncope is a transient, self-limited loss of consciousness due to acute global impairment of cerebral blood flow. The onset is rapid, duration brief, and recovery
spontaneous and complete.
A syncopal prodrome (presyncope) is common, although LOC may occur without warning.
Typical presyncopal symptoms include dizziness, lightheadedness or faintness,
weakness, fatigue, and visual, auditory disturbances.
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Pathophysiological basis
Gradual failure of cerebral perfusion, with a reduction in cerebral oxygen availability.
Cerebral perfusion/oxygenation cut off for 8–10 s, then loss of consciousness and postural tone, pallor and sweating, brief (lasting seconds) extensor stiffening or spasms, few irregular myoclonic jerks of limbs The whole episode is brief, usually <10 s.
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Syncope and age groups
Neurally mediated syncope – MC cause of syncope. slightly higher in females than males. In young subjects- family history in first-degree relatives.
Cardiovascular - in emergency room settings and in older patients.
Syncope due to basilar migraine - more common in young females.
Orthostatic hypotension – increases in prevalence with age because of reduced baroreflex
responsiveness, decreased cardiac compliance, attenuation of the vestibulosympathetic reflex
explained by the greater prevalence of predisposing neurologic disorders, physiologic impairment, and vasoactive medication use among institutionalized patients.
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3 General CategoriesNeurally mediated (also called reflex or vasovagal
syncope) transient change in the reflexes responsible for maintaining
cardiovascular homeostasis. Episodic vasodilation (or loss of vasoconstrictor tone) and
bradycardia occur in varying combinations, resulting in temporary failure of blood pressure control.
Orthostatic hypotension due to autonomic failure: cardiovascular homeostatic reflexes are chronically impaired.
Cardiac syncope: arrhythmias or structural cardiac diseases
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Vasovagal syncope
most common form of neurally mediated syncope,
Results from excessive vagal tone, Abnormal catecholamine response to stress, venous pooling during an upright stance and impaired cardiac filling.
The frequency of vasovagal syncopes varies considerably from one to two during a lifetime to as common as more than once a day.
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C/F of Vasovagal syncope Symptoms of orthostatic intolerance
dizziness, lightheadedness, and fatigue,
premonitory features of autonomic activation diaphoresis, pallor, palpitations, nausea, hyperventilation, and yawning.
During the syncopal event, proximal and distal myoclonus (typically arrhythmic and multifocal) may occur, raising the possibility of epilepsy.
The eyes typically remain open and usually deviate upward. Pupils are usually dilated. Roving eye movements may occur.
Grunting, moaning, snorting, and stertorous breathing may be present. Urinary incontinence may occur. Fecal incontinence is very rare.
Postictal confusion is also rare Although visual and auditory hallucinations and near death and out-of-body experiences are sometimes reported.
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ORTHOSTATIC HYPOTENSION
Defined As: systolic drop at least 20 mmHg or diastolic drop at least 10 mmHg within 3 min of standing or head-up tilt on a tilt table,
Is a manifestation of sympathetic vasoconstrictor (autonomic) failure
In most cases, there is no compensatory increase in HR despite hypotension;
with partial autonomic failure, HR may increase but insufficient to maintain CO
“delayed” orthostatic hypotension, occurs beyond 3 min of
standing; reflects mild or early sympathetic adrenergic dysfunction.
“initial” orthostatic hypotension occurs within 15 s of standing: reflects a transient mismatch between CO and PVR, and does not
represent autonomic failure.
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Upright posture- pooling of 500–1000 mL blood in LL and splanchnic circulation.
decrease in venous return and reduced ventricular filling – diminished CO and BP.
compensatory reflex response, initiated by baroreceptors in carotid sinus, aortic arch: resulting in increased sympathetic outflow decreased vagal nerve activity
This increases peripheral resistance, venous return, and CO and limits the fall in BP.
If this response fails, as in orthostatic hypotension and transiently in neurally mediated syncope, cerebral hypoperfusion occurs.
Cessation of blood flow for 6–8 s will result in LOC, impairment of consciousness -if blood flow < 25 mL/min per 100 g
brain tissue.
Clinically fall in systemic SBP to ~50 mmHg or lower will result in syncope.
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Characteristic symptoms of Orthostatic hypotension
lightheadedness, dizziness, and presyncope
nonspecific, such as generalized weakness, fatigue, cognitive slowing, leg buckling, or headache.
Visual blurring - due to retinal or occipital lobe ischemia.
Neck pain, suboccipital, posterior cervical, and shoulder region (the “coat-hanger headache”), - neck muscle ischemia
Orthostatic Dyspnea – VQ mismatch due to inadequate perfusion of ventilated lung apices)
Angina - impaired myocardial perfusion
Symptoms exacerbated by exertion, prolonged standing, increased ambient temperature, or meals.
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Iatrogenic cause of Ortho. HypoTNDrugs may lower peripheral resistance
Alpha-adrenoreceptor antagonists antihypertensive agents of several classes nitrates and other vasodilators; Tricyclic agents phenothiazines
Iatrogenic volume depletion due to diuresis
Volume depletion due to medical causes hemorrhage, vomiting, diarrhea, decreased fluid intake
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Rare causes
Patients with postural tachycardia syndrome (POTS) frequently experience orthostatic symptoms without orthostatic hypotension, but syncope can occur occasionally.
Rarely, SACD, syringomyelia etc damage the descending sympathetic pathways, producing orthostatic hypotension
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San Francisco Syncope rule
CHESS C - CHF H – Hematocrit <30% E – ECG Abnormal S – Shortness of breath S – SBP in triage area <90
should only be applied to patients whom no cause of syncope is identified
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Other causes of Syncope
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Syncope in Special situations
Syncope induced by Valsalva manoeuvre increased intrathoracic pressure limits the venous
return to the heart increases vagal tone,
resulting in decreased cardiac outflow and syncope.
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Micturition syncope
usually in men while standing for nighttime micturition.
Several mechanisms : postural – standing on leaving a warm bed
causing hypotension straining – Valsalva manoeuvre increasing
an already high nocturnal vagal tone, causing bradycardia
emptying bladder – abrupt decrease in stimulus to bladder stretch receptors causing reflex vasodilatation and hypotension.
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Carotid sinus syncope
Common cause of unexplained falls in elderly>50 years, increses with age
Activation of one or both carotid sinuses causes peripheral vasodilation, hypotension and syncope in carotid sinus hypersensitivity.
Clinical attacks of are attributed to carotid sinus pressure by head turning or tight collars.
Diagnostic carotid sinus massage may be positive in asymptomatic elderly patients but carries a risk of prolonged asystole, transient or permanent neurological deficit, stroke and sudden death.
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Cough (tussive) syncope
LOC occurs after a paroxysm of severe coughing, most likely in obese men (smokers or chronic bronchitis)
Before losing consciousness, the patient may feel lightheaded.
face becomes flushed secondary to congestion, then pale.
Diaphoresis loss of muscle tone
Several factors blockage of venous return by raised intrathoracic
pressure.
weight-lifting syncope - similar mechanism
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Hypoglycemic syncope
Hypoadrenalism - syncope orthostatic hypotension.
Disturbances of Ca, Mg, K metabolism: rare causes
Anoxic syncope- occurs d/t lack of oxygen or production of vasodepressor
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EEG changes in syncopal subjects(2 patterns)
“Slow-flat-slow” pattern normal background activity is replaced with high-amplitude slow delta.
This is followed by sudden flattening of the EEG—a cessation or attenuation of cortical activity—followed by the return of slow waves, and then normal activity.
“Slow pattern,” is characterized by increasing and decreasing slow wave activity only
EEG flattening in the slow-flat-slow pattern denotes severe cerebral hypoperfusion.
Despite the presence of myoclonic movements and other motor activity during some syncopal events, EEG seizure discharges are not detected.
Convulsive syncope is a term used for any type of syncope manifesting with convulsive movements.
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Seizure types that must be distinguished from syncope
Orbitofrontal complex partial seizures, associated with autonomic
changes
Temporal lobe syncope complex partial seizures with sudden falls and altered
awareness, followed by confusion and gradual recovery
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Syncopal attacks provoking epileptic seizures
Anoxic epileptic seizures Occasionally, true epileptic seizures are triggered by
nonepileptic syncopes in children and adults. This combination of syncope and epileptic seizure is
called an anoxic epileptic seizure
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Epileptic seizures imitating syncope
Epileptic seizures may manifest with syncopal likeattacks – “ictal syncope” in Panayiotopoulos syndrome
‘Ictal syncope’ is used to describe this state, because ‘unresponsiveness with loss of postural tone’ is the defining clinical symptom of syncope.
She complained of ‘dizziness’ and then her eyes deviated to the left, she fell on the floor and she became totally flaccid and unresponsive for 5 minutes
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Differential diagnosis of Blackouts
• Syncope • Epilepsy • Psychogenic non-epileptic seizures •Cataplexy Drop attack• Transient CSF obstruction • Transient ischaemic attack - anterior and posterior circulation • Panic attack, • Falls / trauma• Hypoglycaemia • Basilar migraineMalingeeringIntoxication
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APPROACHCareful history
Full a description as possible of the first faint Precipitating factors, posture, type of onset of the faint (abrupt or gradual), position of head and neck, the presence and duration of preceding and associated symptoms, duration of loss of consciousness, rate of recovery, and sequelae.
question an observer about clonic movements, color changes, diaphoresis, pulse, respiration, urinary incontinence, nature of recovery.
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Clinical examinationValsalva maneuverOrthostatic dropAssess BP in both arms when suspecting
cerebrovascular disease, subclavian steal, or Takayasu arteritis.
Pulse: rate and rhythmExtra Cardiac Ascultation: carotid,
ophthalmic, and supraclavicular bruitsCarotid sinus massage in older patients
suspected of having carotid sinus syncope The response to carotid massage is
vasodepressor, cardioinhibitory, or mixed
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InvestigationsDoppler flow of cerebral vessels MRAEEG has a low diagnostic yield
To do only when a seizure disorder is suspectedTilt-table testing in unexplained syncope in high-risk
settings or with recurrent faints in the absence of heart disease False positives - 10% of healthy persons may faint, specificity -90%
ECGProlonged Holter monitoringImplantable loop recordingsRadionuclide cardiac scanning,Echocardiography
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Treatment of Vasovagal syncope
Reassurance, avoidance of provocative stimuli, and plasma volume expansion with fluid
Isometric counterpressure maneuvers of the limbs (leg crossing or handgrip and arm tensing) to maintain pressure in the autoregulatory zone,
Fludrocortisone, vasoconstricting agents, and beta-adrenoreceptor antagonists no consistent evidence from RCT any pharmacotherapy
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Treatment of Orthostatic hypotension
REMOVE REVERSIBLE CAUSES—----------------usually vasoactive medications
NONPHARMACOLOGIC INTERVENTIONS education : staged moves from supine to upright; Warnings about the hypotensive effects of large meals; isometric counterpressure maneuvers that increase intravascular pressure raising the head of the bed to reduce supine hypertension. Intravascular volume expansion : fluid and salt.
PHARMACOLOGIC INTERVENTION fludrocortisone acetate
vasoconstricting agents -midodrine, l-dihydroxyphenylserine, pseudoephedrine
INTRACTABLE SYMPTOMS pyridostigmine, yohimbine, desmopressin erythropoietin
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Treatment of cardiac syncope-
Treatment of underlying disorder. cardiac pacing for sinus node disease and AV block, ablation, antiarrhythmic drugs, and cardioverter-defibrillators
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References
Bradley 7th edtnHarrison 19th edtnPanayiotopoulos 2nd edtnEssential Neurology 4th edtn
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