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Syncope

Chapter 23 | Part 2: Cardinal Manifestations and Presentation of Diseases · Part 2 – Cardinal Manifestations & Presentation · Chapter 23

Key Clinical Points

  1. Syncope is a transient, self-limited loss of consciousness (TLOC) due to acute global impairment of cerebral blood flow.
  2. Three main categories: Neurally mediated syncope, Orthostatic hypotension, and Cardiac syncope.
  3. High-risk features for hospitalization include chest pain, structural heart disease, prolonged QT interval (>500 ms), and history of ventricular arrhythmias (Table 23-1).
  4. Neurally mediated syncope is the most common cause in young subjects; cardiovascular disease is the next most common cause in older patients.
  5. Orthostatic hypotension is 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.
  6. Management of neurally mediated syncope includes reassurance, education, avoidance of triggers, fluid/salt, and isometric counterpressure maneuvers.
  7. Cardiac syncope requires evaluation for arrhythmias and structural disease; treatment depends on the underlying disorder (pacing, ablation, drugs).
  8. Orthostatic hypotension treatment involves removing reversible causes, non-pharmacologic measures, and pharmacologic agents like fludrocortisone or midodrine.
  9. EEG flattening during syncope is a marker of more severity cerebral hypoperfusion; myoclonic movements do not indicate seizure.
  10. Fecal incontinence is very rare with syncope, whereas urinary incontinence may occur.

1. DEFINITION & OVERVIEW

• Definition: Syncope is a transient, self-limited loss of consciousness (TLOC) due to acute global impairment of cerebral blood flow. • Clinical Characteristics: ◦ Rapid onset, brief duration, and spontaneous/complete recovery. ◦ Must be distinguished from other causes of TLOC: seizures, vertebrobasilar ischemia, hypoxemia, and hypoglycemia. • Presyncope: Common but may occur without warning symptoms. ◦ Symptoms include lightheadedness, faintness, dizziness, weakness, fatigue, and visual/auditory disturbances. • Pathophysiology of Cerebral Blood Flow: ◦ Autoregulation: Mediated by myogenic factors, local metabolites, and autonomic neurovascular control (latency 5–10 s). ◦ Normal flow: 50–60 mL/min per 100 g brain tissue; remains constant over perfusion pressures of 50–150 mmHg. ◦ Impairment: Occurs when blood flow drops to 25 mL/min per 100 g brain tissue. ◦ Clinical threshold: Systolic blood pressure ≈ 50 mmHg or lower typically results in syncope. • Hemodynamic Determinants: ◦ Reduced Cardiac Output (CO): Duee to decreased volume, increased thoracic pressure, pulmonary embolism, arrhythmias, valvular disease, or myocardial dysfunction. ◦ Reduced Systemic Vascular Resistance (SVR): Due to autonomic diseases, sympatholytic medications, or transiently during neurally mediated syncope. ◦ Increased Cerebral Vascular Resistance: Often due to hypocarbia from hyperventilation.

2. EPIDEMIOLOGY

• Prevalence: ◦ ~3% of all emergency department (ED) visits; 1% of all hospital admissions. ◦ Annual cost for syncope-related hospitalization in the US: ≈ $2.4 billion. ◦ Lifetime cumulative incidence up to 40% in the general population. • Age Distribution: ◦ Young (10–30 years): Peak at ~15 years; predominantly neurally mediated syncope. ◦ Older (>70 years): Sharp rise in incidence; more likely to be cardiac or orthostatic hypotension. • Prognosis: ◦ Neurally mediated: Excellent prognosis; life expectancy unaffected. ◦ Cardiac/Orthostatic (elderly): Increased risk of sudden cardiac death and mortality from comorbid conditions. • Risk Factors: ◦ Higher incidence in women than men. ◦ Family history in first-degree relatives common in young subjects.

3. ETIOLOGY & PATHOPHYSIOLOGY

• Baroreflex Mechanism (Figure 23-1): ◦ Detection: Baroreceptors in carotid sinus and aortic arch. ◦ Pathway: Afferent fibers → Nucleus of the Tractus Solitarius (NTS) → RVLM (symperatic activation via disinhibition) and NA (parasympathetic reduction). ◦ Hormonal Response: Vasopressin release mediated by A1 noradrenergic cell group in ventrolateral medulla. • Neurally Mediated Syncope: ◦ Requires a functioning autonomic nervous system. ◦ Subtypes: ◦ Vasovagal syncope: Triggered by emotion, pain, or orthostatic stress. ◦ Situational reflex syncopes: Pulmonary (cough, wind instruments), Gastrointestinal (swallow, rectal exam), Urogenital (postmicturition, instrumentation), Heart, Carotid sinus, and Ocular (pressure, surgery). ◦ Vasodepressor syncope: Predominantly efferent, sympathetic, vasoconstrictor failure. ◦ Cardioinhibitory syncope: Predominantly bradycardia or asystole due to increased vagal outflow. ◦ Mixed response syncope: Both vagal and sympathetic reflex changes. • Orthostatic Hypotension (OH): ◦ Definition: ≥ 20 mmHg systolic or ≥ 10 mmHg diastolic drop after 3 min of standing. ◦ Initial OH: <15 s onset, resolve in <45 s; reflects transient mismatch, not autonomic failure. ◦ Delayed OH: Occurs >3 min; reflects mild/early sympathetic dysfunction. ◦ Causes of Autonomic Failure: ◦ Synucleinopathies: Lewy body diseases, Parkinson's disease, Multiple system atrophy (Shy-Drager). ◦ Peripheral Neuropathies: Diabetes, Hereditary amyloidosis, HSAN (especially type III), Sjögren’s syndrome. ◦ Postprandial Hypotension: Exacerbated by large meals, high carbohydrate, and alcohol. • Cardiac Syncope: ◦ Arrhythmias: Sinus node dysfunction, AV dysfunction, SVT, VT, and inherited channelopathies. ◦ Structural Disease: Valvular disease, myocardial ischemia, cardiomyopathy (hypertrophic/other), atrial myxoma, pericardial effusions/tamponade.

4. CLINICAL FEATURES

• Premonitory Features (Neurally Mediated): ◦ Diaphoresis, pallor, palpitations, nausea, hyperventilation, and yawning. • During Syncopal Event: ◦ Myoclonic movements: Typically arrhythmic; do not indicate seizure. ◦ Eyes: Usually open, deviate upward; pupils dilated; roving eye movements may occur. ◦ Respiratory: Grunting, moaning, snorting, or stertorous breathing. ◦ Incontinence: Urinary incontinence possible; fecal incontinence very rare. • Post-event: ◦ Postictal confusion is rare; hallucinations/out-of-body experiences are occasionally reported.

5. DIFFERENTIAL DIAGNOSIS

• Seizures: ◦ Distinction: Myoclonic movements in syncope are arrhythmic; seizures have prolonged postictal state. • Vertebrobasilar Ischemia: Must be distinguished from syncopal events. • Hypoxemia: Must be distinguished from syncopal events. • Hypoglycemia: Must be distinguished from syncopal events.

6. INVESTIGATIONS & DIAGNOSIS

• Electrocardiogram (ECG): ◦ Used to identify high-risk features (Table 23-1) such as QT interval, QRS duration, and arrhythmias. • Electroencephalogram (EEG): ◦ Slow-flat-slow pattern: Normal activity → slow delta waves → sudden flattening (marker of severe hypoperfusion) → return to normal. ◦ Slow pattern: Increasing/decreasing slow wave activity only. ◦ Note: Myoclonic movements do not produce seizure discharges.

7. MANAGEMENT & TREATMENT

  1. Neurally Mediated Syncope: ◦ Education: Reassurance and education regarding triggers. ◦ Lifestyle: Avoidance of known triggers. ◦ Volume Expansion: Fluid and salt (cornerstones of management). ◦ Physical Maneuvers: Isometric counterpressure maneuvers (abdominal/upper muscle tensing is most effective; others include handgrip, arm tensing, leg crossing).
  2. Orthostatic Hypotension: ◦ Primary Step: Identify and remove reversible causes. ◦ Non-pharmacologic: Lifestyle modifications. ◦ Pharmacotherapy: Fludrocortisone or midodrine.
  3. Cardiac Syncope: ◦ Evaluation: Assess for arrhythmias and structural heart disease. ◦ Intervention: Treatment depends on underlying disorder (pacing, ablation, drugs).

8. PROGNOSIS & COMPLICATIONS

• Neurally Mediated: Excellent prognosis; life expectancy unaffected. ◦ Cardiac/Orthostatic (Elderly): Increased risk of sudden cardiac death and mortality from comorbid conditions.

9. SPECIAL CONSIDERATIONS

• Iatrogenic Factors: Orthostatic hypotension often caused by drugs (alpha-blockers, diuretics, nitrates) or volume depletion. ◦ Postprandial Hypotension: Common in patients with autonomic failure; exacerbated by high carbohydrate intake.

10. KEY PEARLS & CLINICAL TRAPS

• High-Risk Features (Table 23-1): ◦ Chest pain (coronary ischemia), Heart failure features, Valvular disease, Structural heart disease. ◦ ECG findings: Ischemia, QT ≥ 500 ms, QRS ≥ 120 ms, Bradycardia, AFib, NSVT. ◦ Other: Family history of sudden death, Brugada pattern, Palpitations at time of syncope, Syncope at rest/exercise. • Myoclonus: Does not indicate seizure; typically arrhythmic in syncopal events. ◦ Orthostatic Definition: ≥ 20 mmHg systolic or ≥ 10 mmHg diastolic drop after 3 min standing. ◦ Synucleinopathies: Includes Lewy body diseases, Parkinson's, and MSA.

Reference Tables

TABLE 23-1 High-Risk Features Indicating Hospitalization or Intensive Evaluation of Syncope Chest pain suggesting…

Harrison's 22e, p.156

  • Chest pain suggesting coronary ischemia
  • Features of congestive heart failure
  • Moderate or severe valvular disease
  • Moderate or severe structural cardiac disease
  • Electrocardiographic features of ischemia
  • History of ventricular arrhythmias
  • Prolonged QT interval (>500 ms)
  • Repetitive sinoatrial block or sinus pauses
  • Persistent sinus bradycardia
  • Bi- or trifascicular block or intraventricular conduction delay with QRS
    duration ≥120 ms
  • Atrial fibrillation
  • Nonsustained ventricular tachycardia
  • Family history of sudden death
  • Preexcitation syndromes
  • Brugada pattern on electrocardiogram
  • Palpitations at time of syncope
  • Syncope at rest or during exercise

TABLE 23-2 Causes of Syncope A. Neurally Mediated Syncope

Harrison's 22e, p.158

  • A. Neurally Mediated Syncope
  • Vasovagal syncope
  • Provoked fear, pain, anxiety, intense emotion, sight of blood, unpleasant
    sights and odors, orthostatic stress
  • Situational reflex syncope
  • Pulmonary
  • Cough syncope, wind instrument player’s syncope, weightlifter’s syncope,
    “mess trick”a and “fainting lark,”b sneeze syncope, airway instrumentation
  • Urogenital
  • Postmicturition syncope, urogenital tract instrumentation, prostatic
    massage
  • Gastrointestinal
  • Swallow syncope, glossopharyngeal neuralgia, esophageal stimulation,
    gastrointestinal tract instrumentation, rectal examination, defecation
    syncope
  • Cardiac
  • Bezold-Jarisch reflex, cardiac outflow obstruction
  • Carotid sinus
  • Carotid sinus sensitivity, carotid sinus massage
  • Ocular
  • Ocular pressure, ocular examination, ocular surgery
  • B. Orthostatic Hypotension
  • Primary autonomic failure due to idiopathic central and peripheral
    neurodegenerative diseases—the “synucleinopathies”
  • Lewy body diseases
  • Parkinson’s disease
  • Lewy body dementia
  • Pure autonomic failure
  • Multiple system atrophy (Shy-Drager syndrome)
  • Secondary autonomic failure due to autonomic peripheral neuropathies
  • Diabetes
  • Hereditary amyloidosis (familial amyloid polyneuropathy)
  • Primary amyloidosis (AL amyloidosis; immunoglobulin light chain
    associated)
  • Hereditary sensory and autonomic neuropathies (HSAN) (especially
    type III—familial dysautonomia)
  • Idiopathic immune-mediated autonomic neuropathy
  • Autoimmune autonomic ganglionopathy
  • Sjögren’s syndrome
  • Paraneoplastic autonomic neuropathy
  • HIV neuropathy
  • Postprandial hypotension
  • Iatrogenic (drug-induced)
  • Volume depletion
  • C. Cardiac Syncope
  • Arrhythmias
  • Sinus node dysfunction
  • Atrioventricular dysfunction
  • Supraventricular tachycardias
  • Ventricular tachycardias
  • Inherited channelopathies
  • Cardiac structural disease
  • Valvular disease
  • Myocardial ischemia
  • Obstructive and other cardiomyopathies
  • Atrial myxoma
  • Pericardial effusions and tamponade