Approach to a Patient with Syncope

-Dr. Sachin Adukia

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.

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.

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.

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

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.

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.

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.

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.

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.

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

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

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

Other causes of Syncope

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.

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.

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.

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

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

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.

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

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

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

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

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.

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

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

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

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

Treatment of cardiac syncope-

Treatment of underlying disorder. cardiac pacing for sinus node disease and AV block, ablation, antiarrhythmic drugs, and cardioverter-defibrillators

References

Bradley 7th edtnHarrison 19th edtnPanayiotopoulos 2nd edtnEssential Neurology 4th edtn

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