CHAPTER
15
Syncope
UNDERSTANDING AND MANAGING SYNCOPE
Syncope is defined as a sudden, transient loss of consciousness and postural tone with spontaneous recovery.
○Incidence of syncope is 6.2/1000 person years with a 30% recurrence.
○Syncope accounts for 3% of emergency room (ER) visits and 1%–6% of hospital admissions.
○If the cause of syncope is cardiac, there is a 20% 1-year mortality rate.
Etiology
○Cardiac causes (20%)
▪ Arrhythmia
• Tachyarrhythmia: Supraventricular tachycardia (SVT), atrial fibrillation (AF)/atrial flutter (AFL), ventricular tachycardia (VT)
• Bradyarrhythmia: Bradycardia, AV block, or bundle branch block (BBB)
▪ Mechanical obstruction
• Valvular: Aortic stenosis, pulmonary stenosis, mitral stenosis
• Hypertrophic obstructive cardiomyopathy
• Pump failure: MI, tamponade
• Other: Atrial myxoma, pulmonary embolism
○Neurocardiogenic causes (60%)
▪ Pathophysiology (Bezold-Jarisch reflex)
• Peripheral venous pooling results in a drop in preload triggering a hypercontractile state. This results in mechanoreceptor stimulation (posterior-inferior LV) triggering a medullary vasodepressor brain stem reflex. This results in decreased sympathetic and increased vagal tone, leading to lower heart rate (HR), blood pressure (BP), and blood vessel tone.
▪ Subtypes:
• Carotid sinus hypersensitivity (lower BP, lower HR, or both)
• Vasovagal syncope: “Common faint,” cardioinhibitory, and vasodepressor variants
• Situational syncope: Micturition, defecation, deglutition, cough, swallow, pain
▪ Vertebrobasilar insufficiency, usually associated with dysarthria and dysphagia
▪ Subarachnoid haemorrhage
▪ Seizure (bicortical failure): Sudden loss of postural tone followed by tonic-clonic movements. Incontinence and post-event confusion are common.
▪ Atypical migraine
○Orthostatic hypotension
▪ Pathophysiology: Postural hypotension resulting in symptoms of cerebral hypoperfusion, leading to decreased effective circulating volume
▪ Potential causes include:
• Volume depletion due to hemorrhage, diuresis, diarrhea, sepsis, salt wasting, and supine hypertension
• Hyperthyroid, diabetes (hyperglycemia), pheochromocytoma, adrenal insufficiency, diabetes insipidus (DI)
• Venous pooling: Postural, morning, postprandial, pregnancy
○Drugs
▪ Antihypertensive (sympatholytic, vasodilator, diuretic), nitrates, alcohol
▪ Antidepressant (tricyclic antidepressant [TCA]), antipsychotic, anti-Parkinsonian drugs, benzodiazepines, narcotics
▪ Autonomic neuropathy (diabetes mellitus, alcohol, B12, amyloid, Bradbury-Eggleston, Shy-Drager)
▪ Neurologic (stroke, posterior fossa tumours, upper cervical cord lesions)
○Other
▪ Psychiatric: Somatization, pain, anxiety
▪ Metabolic: Hypoglycemia, dumping syndrome, hypoxia, hypocapnea
Clinical
○History/physical examination is diagnostic in 40%–50% (50% of cases are undiagnosed).
○Structured history may help improve the diagnostic yield, and is evidence-based:
▪ Calgary syncope score (Eur Heart J. 2006;3:344–350); vasovagal syncope if score ≥ –2; see Table 15.1
Table 15.1 Calgary Syncope Score
| Component | Score |
1. History of bifascicular block, asystole, SVT, diabetes | –5 |
2. History of bystanders noting a bluish skin tone during the episode | –4 |
3. Syncope beginning after the age of 35 years | –3 |
4. Do you remember anything about being unconscious | –2 |
5. Lightheaded spells or fainting with prolonged sitting or standing | 1 |
6. Do you sweat or feel warm before a faint? | 2 |
7. Do you have lightheaded spells or faint with pain or in medical settings? | 3 |
▪ Young
• Predominantly these cases are vasovagal.
• Uncommon causes such as idiopathic VT, prolonged QT, and HCM should be considered with an atypical history.
▪ Older
• Strongly consider an arrhythmic cause.
○Number of episodes
▪ Single/multiple over long period (~benign)
▪ Multiple over short period (~malignant)
Table 15.2 Characteristics of Syncope Episodes that Point to Neurocardiogenic vs. Arrhythmia
| Neurocardiogenic | Arrhythmia | |
Triggers | Prolonged standing Pain, emotional upset, fear/anxiety CSH: Turning head, seat belt, shaving Situation: Defecation, coughing, eating, drinking | Seated or supine |
Prodrome | Nausea, diaphoresis, presyncope Pallor, palpitations, visual changes | Sudden LOC without warning |
Onset – Offset | Abrupt – Slow | Abrupt – Abrupt |
Resolution | Immediately after lying down | |
Residual symptoms | Fatigue/weakness (usually severe), nausea Diaphoresis, headache |
CSH: carotid sinus hypersensitivity; LOC: loss of consciousness.
○Medical history
▪ Diabetes
▪ Psychiatric disorders
▪ Coronary arterial disease (CAD) (if present, then 26% chance cardiac syncope; if absent, then 24% vasovagal syncope)
○Medications/drugs (especially changes):
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