Understanding Syncope: Causes, Diagnosis, and Management

• Syncope is a temporary loss of consciousness and postural tone.
• Syncope is caused by global cerebral hypoperfusion, followed by spontaneous and complete recovery.
• Syncope accounts for 1-3% of emergency department visits and up to 6% of hospital admissions.
• Syncope can be caused by several factors, including cardiac, neurological, and vasovagal mechanisms.
• Syncope requires proper evaluation and management and can be a sign of serious underlying conditions.
• Syncope is a transient, self-limited loss of consciousness due to acute global impairment of cerebral blood flow.
• The characteristics of syncope are rapid onset, brief duration, and spontaneous and complete recovery.
• Conditions that need to be distinguished from syncope Loss of consciousness include seizures, vertebrobasilar ischemia, hypoxemia, and hypoglycemia.
• A syncopal prodrome (presyncope) is common.
• Loss of consciousness may occur without any warning symptoms.
• Lightheadedness, faintness, dizziness, weakness, fatigue, and visual and auditory disturbances are typical presyncopal symptoms.
• Syncope has three general categories: neurally mediated syncope (reflex or vasovagal syncope), orthostatic hypotension, and cardiac syncope.
• Neurally mediated syncope is a heterogeneous group of functional disorders characterized by a transient change in the reflexes responsible for maintaining cardiovascular homeostasis.
• Episodic vasodilation (or loss of vasoconstrictor tone), decreased cardiac output, and bradycardia occur in varying combinations, resulting in temporary failure of blood pressure control.
• In patients with orthostatic hypotension due to autonomic failure, cardiovascular homeostatic reflexes are chronically impaired.
• Cardiac syncope may be due to arrhythmias or structural cardiac diseases that cause a decrease in cardiac output.
• Clinical features, underlying pathophysiologic mechanisms, therapeutic interventions, and prognoses differ among these three causes.
• Syncope is a common presenting problem, accounting for ~3% of all emergency department (ED) visits and 1% of all hospital admissions.
• The annual cost for syncope-related hospitalization in the United States is ~$2.4 billion.
• Syncope has a lifetime cumulative incidence of up to 35% in the general population.
• The peak incidence in the young occurs between ages 10 and 30 years, with a median peak around 15 years.
• Neurally mediated syncope is the etiology in the vast majority of these cases.
• In older adults, there is a sharp rise in the incidence of syncope after 70 years of age.
• In population-based studies, neurally mediated syncope is the most common cause of syncope.
• The incidence of syncope is higher in women than men.
• In young subjects, there is often a family history in first-degree relatives.
• Cardiovascular disease due to structural disease or arrhythmias is the next most common cause in most series, particularly in ED settings and in older patients.
• Orthostatic hypotension also increases in prevalence with age because of the reduced baroreflex responsiveness, decreased cardiac compliance, and attenuation of the vestibulosympathetic reflex associated with aging.
• Reduced fluid intake and vasoactive medications are the other contributors to orthostatic hypotension.
• Orthostatic hypotension is more common in institutionalized elderly patients than in community-dwelling individuals.
• Syncope of noncardiac and unexplained origin in younger individuals has an excellent prognosis, and life expectancy is unaffected.
• Syncope due to a cardiac cause, either structural heart disease or a primary arrhythmic disorder, is associated with an increased risk of sudden cardiac death and mortality from other causes.
• The mortality rate is increased in individuals with syncope due to orthostatic hypotension related to age and the associated comorbid conditions.
• The likelihood of hospitalization and mortality risk are higher in older adults.
• Syncope occurs due to a sudden drop in cerebral blood flow, typically lasting 3-5 seconds.
• The main categories of syncope include reflex (neurally-mediated), orthostatic hypotension, and cardiac syncope.
• Reflex syncope, aka vasovagal syncope, is the most common type and is caused by an inappropriate autonomic response.
• Cardiac syncope may result from arrhythmias, structural heart disease, or other cardiovascular conditions.
• The upright posture imposes a unique physiologic stress upon humans; most, although not all, syncopal episodes occur from a standing position.
• Standing results in pooling of 500-1000 mL of blood in the lower extremities, buttocks, and splanchnic circulation
• The dependent pooling leads to a decrease in venous return to the heart and reduced ventricular filling that result in diminished cardiac output and blood pressure.
• These hemodynamic changes provoke a compensatory reflex response, initiated by the baroreceptors in the carotid sinus and aortic arch, resulting in increased sympathetic outflow and decreased vagal nerve activity
• The reflex increases peripheral resistance, venous return to the heart, and cardiac output and thus limits the fall in blood pressure.
• Hypotension and cerebral hypoperfusion occur if cardiovascular reflexes fail, as chronically in orthostatic hypotension and transiently in neurally mediated syncope.
• Syncope is a consequence of global cerebral hypoperfusion, thus representing a failure of cerebral blood flow autoregulatory mechanisms.
• Myogenic factors, local metabolites, and autonomic neurovascular control are responsible for the autoregulation of cerebral blood flow
• The latency of the autoregulatory response is 5-10 s.
• Cerebral blood flow ranges from 50–60 mL/min per 100 g brain tissue and remains relatively constant over perfusion pressures ranging from 50-150 mmHg.
• Cessation of blood flow for 6–8 s will result in loss of consciousness.
• Impairment of consciousness ensues when blood flow decreases to 25 mL/min per 100 g brain tissue.
• A fall in systemic systolic blood pressure to ~50 mmHg or lower will result in syncope.
• A decrease in cardiac output and/or systemic vascular resistance underlies the pathophysiology of syncope.
• Common causes of impaired cardiac output include decreased effective circulating blood volume, increased thoracic pressure, massive pulmonary embolus, cardiac brady- and tachyarrhythmias, valvular heart disease, and myocardial dysfunction.
• Systemic vascular resistance may be decreased by central and peripheral autonomic nervous system diseases, sympatholytic medications, and transiently during neurally mediated syncope.
• Increased cerebral vascular resistance, most frequently due to hypocarbia induced by hyperventilation, may also contribute to the pathophysiology of syncope.
• Two patterns of electroencephalographic (EEG) changes occur in syncopal subjects.
• The first is a “slow-flat-slow” pattern in which normal background activity is replaced with high-amplitude slow delta waves, followed by sudden flattening of the EEG, followed by the return of slow waves, and then normal activity.
• The second pattern, the “slow pattern,” is characterized by increasing and decreasing slow wave activity only.
• The EEG flattening that occurs in the slow-flat-slow pattern is a marker of more severe cerebral hypoperfusion.
• EEG seizure discharges are not detected despite the presence of myoclonic movements and other motor activity during some syncopal events.

3 Most Common Causes of Syncope

• Neurally Mediated Syncope is the most common type, which is seen primarily in younger adults.
• A reflex response causes vasodilation, bradycardia, and systemic hypotension, leading to decreased blood flow.
• Neurally mediated (reflex; vasovagal) syncope is the final pathway of a complex central and peripheral nervous system reflex arc.
• A transient change in autonomic efferent activity with increased parasympathetic outflow, plus sympathoinhibition, results in bradycardia, vasodilation, reduced vasoconstrictor tone (the vasodepressor response) and reduced cardiac output.
• The resulting fall in systemic blood pressure can then reduce cerebral blood flow to below the compensatory limits of autoregulation.
• A functioning autonomic nervous system is necessary to develop neurally mediated syncope, in contrast to syncope resulting from autonomic failure
• Multiple triggers of the afferent limb of the reflex arc can result in neurally mediated syncope.
• Orthostatic stress and stimulus of the carotid sinus, the gastrointestinal tract, or the bladder can be triggers
• Different afferent pathways converge on the central autonomic network within the medulla that integrates the neural impulses and mediates the vasodepressor-bradycardic response.
• Neurally mediated syncope may be subdivided based on the afferent pathway and provocative trigger.
• Vasovagal syncope (the common faint) is provoked by intense emotion, pain, and/or orthostatic stress.
• Situational reflex syncopes have specific localized stimuli that provoke the reflex vasodilation and bradycardia that leads to syncope.
• The underlying mechanisms have been identified, and pathophysiology delineated for most of these situational reflex syncopes.
• The afferent trigger may originate in the pulmonary system, gastrointestinal system, urogenital system, heart, and carotid sinus in the carotid artery.
• Hyperventilation leading to hypocarbia and cerebral vasoconstriction, and raised intrathoracic pressure that impairs venous return to the heart, play a central role in many situational reflex syncopes.
• The afferent pathway of the reflex arc differs among these disorders, but the efferent response via the vagus and sympathetic pathways is similar.
• Neurally mediated syncope may be subdivided based on the predominant efferent pathway.
• Vasodepressor syncope describes syncope predominantly due to efferent, sympathetic, vasoconstrictor failure.
• Cardioinhibitory syncope describes syncope predominantly associated and sympathetic reflex changes.

Features of Neurally Mediated Syncope

• In addition to symptoms of orthostatic intolerance such as dizziness, lightheadedness, and fatigue, premonitory features of autonomic activation may be present.
• These premonitory signs include diaphoresis, pallor, palpitations, nausea, hyperventilation, and yawning.
• Proximal and distal myoclonus (typically arrhythmic and multifocal) may occur during the syncopal event, raising the possibility of a seizure.
• 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, however.
• Postictal confusion is also rare, although visual and auditory hallucinations and neardeath and out-of-body experiences are sometimes reported.
• Motionless upright posture, warm ambient temperature, intravascular volume depletion, alcohol ingestion, hypoxemia, anemia, pain, the sight of blood, venipuncture, and intense emotion are predisposing factors and provocative stimuli.
• The underlying basis for the widely different thresholds for syncope among individuals exposed to the same provocative stimulus is not known.
• A genetic basis for neurally mediated syncope may exist; in first-degree relatives of fainters the incidence of syncope is higher.
• Environmental, social, and cultural factors may, with bradycardia or asystole due to increased vagal outflow may contribute to syncope.

Specific causes of Neurally Mediated Syncope- vasovagal

• Vasovagal syncope is mediated by stress, fear, noxious stimuli, or heat exposure
• Situational syncope is caused my Micturition, post-exercise, postprandial, GI stimulation, cough, phobia of needle or blood
• Carotid sinus syndrome hypersensitivity is cause by head rotation or pressure on the carotid shaving and wearing tight collars.
• Cardiac: The 2nd most common type.
• The Elderly: Generally seen in older adults.
• The cause: Results from arrhythmias, mechanical or structural abnormalities.
• Often unprovoked and more likely to present in the ED
• Sudden death in young adults with syncope: Sudden death in young adults with syncope is often the result of arrhythmias.
• Arrhythmia: Arrythmias include: Bradyarrhythmias, ventricular tachyarrhythmias, supraventricular tachyarrhythmias, long QT syndrome, pacemaker dysfunction
• Obstructive cardiomyopathy: Cause- Hypertrophic cardiomyopathy
• Structural disease (cardiac): Causes- Aortic stenosis, pulmonary stenosis, acute MI, Ischemia
• Structural disease (other): Pulmonary hypertension, pulmonary embolus, acute aortic dissection

CARDIAC SYNCOPE

• Cardiac syncope is caused by arrhythmias and structural heart disease.
• These may occur in combination because structural disease renders the heart more vulnerable to abnormal electrical activity.
• Bradyarrhythmias that cause syncope include those due to severe sinus node dysfunction (e.g., sinus arrest or sinoatrial block) and atrioventricular (AV) block (e.g., Mobitz type II, highgrade, and complete AV block).
• The bradyarrhythmias due to sinus node dysfunction are often associated with an atrial tachyarrhythmia, a disorder known as the tachycardia-bradycardia syndrome.
• A prolonged pause following the termination of a tachycardic episode is a frequent cause of syncope in patients with the tachycardia-bradycardia syndrome.
• Medications of several classes may also cause bradyarrhythmias of sufficient severity to cause syncope.
• Syncope due to bradycardia or asystole has been referred to as a Stokes-Adams attack.
• Ventricular tachyarrhythmias frequently cause syncope.
• The likelihood of syncope with ventricular tachycardia is in part dependent on the ventricular rate; rates <200 beats/min are less likely to cause syncope.
• The compromised hemodynamic function during ventricular tachycardia is caused by ineffective ventricular contraction, reduced diastolic filling due to abbreviated filling periods, loss of AV synchrony, and concurrent myocardial ischemia.
• Several disorders associated with cardiac electrophysiologic instability and arrhythmogenesis are due to mutations in ion channel subunit genes.
• These include the long QT syndrome, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia.
• The long QT syndrome is a genetically heterogeneous disorder associated with prolonged cardiac repolarization and a predisposition to ventricular arrhythmias.
• Syncope and sudden death in patients with long QT syndrome result from a unique polymorphic ventricular tachycardia called torsades des pointes that degenerates into ventricular fibrillation.
• The long QT syndrome has been linked to genes encoding K+ channel a-subunits, K+ channel ẞ-subunits, voltage-gated Na+ channel, and a scaffolding protein, ankyrin B (ANK2).
• Brugada syndrome is characterized by idiopathic ventricular fibrillation in association with right ventricular electrocardiogram (ECG) abnormalities without structural heart disease and is also genetically heterogenous.
• Catecholaminergic polymorphic tachycardia is an inherited, genetically heterogeneous disorder associated with exercise- or stress-induced ventricular arrhythmias, syncope, or sudden death.
• Acquired QT interval prolongation, most commonly due to drugs, may also result in ventricular arrhythmias and syncope.
• Structural heart disease may lead to syncope by compromising cardiac output.
• Structural heart diseases include valvular disease, myocardial ischemia, hypertrophic and other cardiomyopathies, cardiac masses such as atrial myxoma, and pericardial effusions
• Structural disease may also contribute to other pathophysiologic mechanisms of syncope.
• Cardiac structural disease may predispose to arrhythmogenesis, aggressive treatment of cardiac failure with diuretics and/or vasodilators may lead to orthostatic hypotension, and inappropriate reflex vasodilation may occur with structural disorders such as aortic stenosis and hypertrophic cardiomyopathy, possibly provoked by increased ventricular contractility.

TREATMENT Cardiac Syncope

• Medical management depends on the underlying disorder.
• Therapies for arrhythmias include cardiac pacing for sinus node disease and AV block, and ablation, antiarrhythmic drugs, and cardioverter-defibrillators for atrial and ventricular tachyarrhythmias.
• These disorders are best managed by physicians with specialized skills in this area.
• Othostatic Hypotension: Defined as a reduction in systolic blood pressure of at least 20 mmHg or diastolic blood pressure of at least 10 mmHg after 3 min of standing or head-up tilt on a tilt table, is a manifestation of sympathetic vasoconstrictor (autonomic) failure .
• In many (but not all) cases, there is no compensatory increase in heart rate despite hypotension; with partial autonomic failure,
• Heart rate may increase to some degree but is insufficient to maintain cardiac output.
• A variant of orthostatic hypotension is “delayed” orthostatic hypotension, which occurs beyond 3 min of standing; this may reflect a mild or early form of sympathetic adrenergic dysfunction.
• In some cases, orthostatic hypotension occurs within 15 s of standing (so-called initial orthostatic hypotension), a finding that may reflect a transient mismatch between cardiac output and peripheral vascular resistance and does not represent autonomic failure.

Characteristic symptoms of orthostatic hypotension include

• Light-headedness, dizziness, and presyncope (near-faintness) occurring in response to sudden postural change.
• Symptoms may also be absent or nonspecific, such as generalized weakness, fatigue, cognitive slowing, leg buckling, or headache.
• Visual blurring may occur, likely due to retinal or occipital lobe ischemia.
• Neck pain, typically in the suboccipital, posterior cervical, and shoulder region (the “coathanger headache"), most likely due to neck muscle ischemia, may be the only symptom.
• Patients may report orthostatic dyspnea (thought to reflect ventilation-perfusion mismatch due to inadequate perfusion of ventilated lung apices) or angina (attributed to impaired myocardial perfusion even with normal coronary arteries).
• Symptoms may be exacerbated by exertion, prolonged standing, increased ambient temperature, or meals.
• Syncope is usually preceded by warning symptoms, but may occur suddenly, suggesting the possibility of a seizure or cardiac cause.
• Some patients have profound decreases in blood pressure, sometimes without symptoms but placing them at risk for falls and injuries if the autoregulatory threshold is crossed with ensuing cerebral hypoperfusion.
• Supine hypertension is common in patients with orthostatic hypotension due to autonomic failure, affecting >50% of patients in some series.
• Orthostatic hypotension may present after initiation of therapy for hypertension, and supine hypertension may follow treatment of orthostatic hypotension.
• The association of the two conditions is unrelated to therapy.
• The association may in part be explained by baroreflex dysfunction in the presence of residual sympathetic outflow, particularly in patients with central autonomic degeneration.

Causes of Neurogenic Orthostatic Hypotension

• Causes of neurogenic orthostatic hypotension include central and peripheral autonomic nervous system dysfunction .
• Autonomic dysfunction of other organ systems (including the bladder, bowels, sexual organs, and the sudomotor system) of varying severity frequently accompanies orthostatic hypotension in these disorders
• The primary autonomic degenerative disorders are multiple system atrophy (Shy-Drager syndrome), Parkinson's disease, dementia with Lewy bodies, and pure autonomic failure.
• These neurodegenerative disorders are often grouped together as “synucleinopathies” due to the presence of a-synuclein, a protein that aggregates predominantly in the cytoplasm of neurons in the Lewy body disorders (Parkinson's disease, dementia with Lewy bodies, and pure autonomic failure) and in the glia in multiple system atrophy.
• Peripheral autonomic dysfunction may also accompany small-fiber peripheral neuropathies such as those associated with diabetes mellitus, acquired and hereditary amyloidosis, immune-mediated neuropathies, and hereditary sensory and autonomic neuropathies (HSAN; particularly HSAN type III, familial dysautonomia)
• Orthostatic hypotension is associated with the peripheral neuropathies that accompany vitamin B12 deficiency, neurotoxin exposure, HIV and other infections, and porphyria.
• Patients with autonomic failure and the elderly are susceptible to falls in blood pressure associated with meals.
• The magnitude of the blood pressure fall is exacerbated by large meals, meals high in carbohydrate, and alcohol intake.

Iatrogenic orthostatic hypotension

• Orthostatic hypotension is often iatrogenic.
• Drugs from several classes may lower peripheral resistance (e.g., a-adrenoreceptor antagonists used to treat hypertension and prostatic hypertrophy; anti-hypertensive agents of several classes; nitrates and other vasodilators; tricyclic agents and phenothiazines).
• Iatrogenic volume depletion due to diuresis and volume depletion due to medical causes (hemorrhage, vomiting, diarrhea, or decreased fluid intake) may also result in decreased effective circulatory volume, orthostatic hypotension, and syncope.

TREATMENT Orthostatic Hypotension

• The first step is to remove reversible causes: vasoactive medications .
• Next, nonpharmacologic interventions should be introduced: Patient education regarding staged moves from supine to upright; warnings about the hypotensive effects of large meals; instructions about the isometric counterpressure maneuvers that increase intravascular pressure and raising the head of the bed to reduce supine hypertension and nocturnal diuresis.
• Intravascular volume should be expanded by increasing dietary fluid and salt.
• If these nonpharmacologic measures fail, pharmacologic intervention with fludrocortisone acetate and vasoconstricting agents such as midodrine and I-dihydroxyphenylserine should be introduced.
• Some patients with intractable symptoms require additional therapy with supplementary agents that include pyridostigmine, atomoxetine, yohimbine, octreotide, desmopressin acetate (DDAVP), and erythropoietin

INCIDENCE OF SYNCOPE

• The annual incidence of syncope is approximately 18.1-39.7 per 1000 patients in the general population.
• Incidence increases significantly with age, rising from 5.7 episodes per 1000 person-years in individuals aged 60-69 to 11.1 episodes per 1000 person-years in those aged 70-79.

RISK FACTORS OF SYNCOPE

• Age: Incidence increases sharply after 70 years of age.
• Cardiovascular conditions: Structural heart disease, arrhythmias, or heart failure increases risk.
• Male gender: Associated with higher risk of cardiac syncope.

PREVENTION OF SYNCOPE

• Regular cardiovascular check-ups, especially for older adults
• Management of underlying cardiovascular conditions
• Avoiding triggers for vasovagal syncope (e.g., prolonged standing, dehydration)
• Proper hydration and gradual position changes for those prone to orthostatic hypotension

CLINICAL MANIFESTATIONS OF SYNCOPE

• Sudden, brief loss of consciousness with spontaneous recovery.
• Prodromal symptoms such as lightheadedness, nausea, or visual disturbances.
• Fall or collapse due to loss of postural tone.
• Rapid return to normal mental status after the event.
• Possible injury from falls during syncopal episodes.

REVIEW OF SYSTEMS

• Cardiovascular: Palpitations, chest pain, dyspnea
• Neurological: Dizziness, visual changes, headache
• Gastrointestinal: Nausea, abdominal discomfort
• Musculoskeletal: Injuries from falls
• Psychological: Anxiety related to syncope episodes

PHYSICAL ASSESSMENT FINDINGS

• Cardiovascular assessment includes irregular heart rhythm or murmurs on auscultation and orthostatic blood pressure changes.
• Neurological assessment: Normal neurological exam between episodes and possible signs of head injury if fall occurred.
• General assessment: Signs of dehydration or volume depletion.

ASSESSMENT TOOLS & GRADING

• San Francisco Syncope Rule: Assesses risk of serious outcomes
• ROSE (Risk Stratification of Syncope in the Emergency Department) criteria
• Canadian Syncope Risk Score

HIGH YIELD QUESTIONS TO ASK PATIENT

• Can you describe what happened before, during, and after the episode?
• Have you had similar episodes before?
• Were there any triggers (e.g., standing up quickly, emotional stress)?
• Did you experience any warning signs before fainting?
• How quickly did you recover consciousness?
• Do you have any known heart conditions?
• Are you taking any medications that could contribute to fainting?
• Did you experience chest pain, palpitations, or shortness of breath?
• Have you had any recent injuries or falls?
• Has anyone in your family experienced unexplained fainting or sudden death?

DIFFERENTIAL DIAGNOSES

• Vasovagal Syncope is Triggered by stressor prolonged standing. Diagnostics Tilt table test
• Cardiac Syncope Is Associated with exertion and heart disease. Diagnostics include ECG and Echocardiogram
• Orthostatic Hypotension Occurs upon standing. Diagnostics: Orthostatic vital signs
• Seizure, prolonged loss of consciousness, post-ictal state. Diagnostics include EEG
• Stroke/TIA includes focal neurological deficits. Diagnostics: Brain imaging (CT/MRI)

DIAGNOSTIC STUDIES & POSSIBLE FINDINGS

• ECG: May show arrhythmias, conduction abnormalities, or signs of structural heart disease. Echocardiogram: Can reveal structural heart abnormalities or valvular disease.
• Tilt table test: Helps diagnose vasovagal syncope by reproducing symptoms.
• Holter monitor: Detects intermittent arrhythmias that may cause syncope.
• Laboratory tests: Assess for anemia, electrolyte imbalances, or cardiac biomarkers.

TREATMENT PRIORITIZATION

• Immediate assessment of airway, breathing, and circulation
• Identification and treatment of underlying cause
• Risk stratification for serious outcomes
• Patient education and prevention strategies
• Follow-up and monitoring for recurrence

TREATMENT: Neurally Mediated Syncope

• Reassurance, education, avoidance of provocative stimuli, and plasma volume expansion with fluid and salt are the cornerstones of the management of neurally mediated syncope.
• Isometric counterpressure maneuvers of the limbs (tensing of the abdominal and leg muscles, handgrip and arm tensing, and leg crossing) may raise blood pressure by increasing central blood volume and cardiac output. Abdominal muscle tensing is the most effective.
• By maintaining pressure in the autoregulatory zone, these maneuvers, which may be particularly helpful in patients with a long prodrome, avoid or delay the onset of syncope.
• Randomized controlled trials support this intervention.
• Fludrocortisone, vasoconstricting agents, and ẞ-adrenoreceptor antagonists are widely used by experts to treat refractory patients, although there is no consistent evidence from randomized controlled trials for any pharmacotherapy to treat neurally mediated syncope.
• Because vasodilation, decreased central blood volume, decreased stroke volume and cardiac output are the dominant pathophysiologic syncopal mechanisms in most patients, use of a cardiac pacemaker is rarely beneficial.
• A systematic review of the literature examining whether cardiac pacing reduces risk of recurrent syncope and relevant clinical outcomes in adults with neurally mediated syncope, concluded that the existing evidence does not support the use of routine cardiac pacing.
• Possible exceptions are (1) older patients (>40 years), with at least three prior episodes associated with asystole (of at least 3 s associated with syncope or at least 6 s associated with presyncope) documented by an implantable loop recorder; and (2) patients with prominent cardioinhibition due to carotid sinus syndrome. In these patients, dual-chamber pacing may be helpful, although this continues to be an area of uncertainty.

SPECIAL CONSIDERATIONS/SPECIFIC CIRCUMSTANCES

• Elderly patients may have multiple contributing factors
• Patients with implantable cardioverter-defibrillators require device interrogation
• Pregnant women may experience increased vasovagal syncope

NONPHARMACOLOGICAL INTERVENTIONS

• Patient education on trigger avoidance and proper hydration
• Physical counterpressure maneuvers for vasovagal syncope
• Compression stockings for orthostatic hypotension
• Cardiac rehabilitation for patients with cardiac syncope

PHARMACOLOGICAL MANAGEMENT

• 1st Line: Beta-blockers for vasovagal syncope (e.g., metoprolol 25-100 mg twice daily)
• 2nd Line: Fludrocortisone for orthostatic hypotension/Autonomic insufficiency- (0.1-0.2 mg daily)
• 3rd Line: Midodrine for refractory orthostatic hypotension (2.5-10 mg three times daily)
• Monitor: Blood pressure, electrolytes, and symptom improvement
• Single or rare episodes of reflex syncope do not require treatment
• Midodrine (alpha agonist) may be considered in patients with frequent hypotensive symptoms
• Starting dose is 5 mg three times a day, Best to 10 mg three times a day, As its duration of action is short (2 to 4 hours).
• Take before arising in the morning, before lunch, and in the midafternoon
• Autonomic insufficiency- Fludrocortisone (Florinef), midodrine (ProAmatine) - Physical Therapy, support stockings.
• Neurocardiogenic syncope causes- Beta blocker, fludrocortisone (Florinef) and salt
• Hypovolemia includes- Fludrocortisone (Florinef), salt

CONSULTATION/REFERRAL for Syncope

• Cardiology for suspected cardiac syncope or arrhythmias
• Neurology for suspected seizures or neurological causes
• Electrophysiology for complex arrhythmias or consideration of pacemaker

INITIAL DIAGNOSIS PATIENT GUIDANCE:

Explain the diagnosis and potential causes

• Discuss trigger avoidance and lifestyle modifications
• Teach physical counterpressure maneuvers if appropriate
• Emphasize the importance of follow-up and reporting new symptoms

FOLLOW UP AND SURVEILLANCE for Syncope

• Schedule follow-up within 1-4 weeks, depending on risk stratification. Monitor for recurrence, medication effectiveness, and emergence of new symptoms. Consider longer-term cardiac monitoring for unexplained syncope.

EXPECTED COURSE:

• Prognosis varies depending on the underlying cause. Many patients with vasovagal syncope have a benign course with proper management. Cardiac syncope may require ongoing treatment and monitoring.

POSSIBLE COMPLICATIONS of syncope

• Injuries from falls during syncopal episodes
• Recurrent syncope (35% recurrence rate)
• Reduced quality of life and anxiety related to unpredictable episodes
• Potential for sudden cardiac death in cases of underlying serious cardiac conditions