What causes syncope in the absence of hypotension (low blood pressure)?

Non-Hypotensive Causes of Syncope

Syncope without documented hypotension most commonly results from cardiac arrhythmias, structural heart disease, or neurally-mediated reflex mechanisms where blood pressure drops too rapidly to measure, though neurogenic orthostatic hypotension with inadequate compensatory responses should also be considered.

Cardiac Arrhythmias

Arrhythmias represent the most critical non-hypotensive cause requiring immediate evaluation:

Bradyarrhythmias

• Sinus bradycardia <40 beats/min 1
• Repetitive sinoatrial blocks or sinus pauses >3 seconds 1
• Mobitz II second-degree or third-degree atrioventricular block 1
• Alternating left and right bundle branch block 1
• Pacemaker malfunction with cardiac pauses 1

Tachyarrhythmias

• Rapid paroxysmal supraventricular tachycardia 1
• Ventricular tachycardia 1
• Paroxysmal atrial tachyarrhythmias (can occur even with normal baseline ECG) 1

Key Point: ECG abnormalities suggesting arrhythmic syncope include bifascicular block, QRS duration ≥0.12s, pre-excited QRS complexes, prolonged QT interval, Brugada pattern (RBBB with ST-elevation V1-V3), and signs of arrhythmogenic right ventricular dysplasia 1.

Structural Cardiac Disease

Structural abnormalities cause syncope through mechanical obstruction and inadequate cardiac output:

Obstructive Lesions

• Aortic stenosis (most common valvular cause) 1
• Hypertrophic obstructive cardiomyopathy 1
• Mitral stenosis or atrial myxoma (left ventricular inflow obstruction) 1
• Pulmonary stenosis or pulmonary hypertension (right-sided obstruction) 1

Acute Cardiac Events

• Acute myocardial ischemia or infarction 1
• Pulmonary embolism 1
• Acute aortic dissection 1
• Pericardial tamponade 1
• Cardiac tumors 1

Critical Caveat: In structural heart disease, syncope often results from multifactorial mechanisms including both hemodynamic compromise AND neurally-mediated reflex effects (especially the Bezold-Jarisch reflex in inferior MI) 1. Even "benign" arrhythmias like atrial fibrillation can precipitate syncope in patients with obstructive lesions 1.

Neurally-Mediated (Reflex) Syncope

These syndromes cause rapid vasodilation and/or bradycardia that may occur too quickly for blood pressure measurement:

Vasovagal Syncope

• Emotional triggers: fear, severe pain, emotional distress, blood phobia 1, 2, 3
• Orthostatic stress: prolonged standing 1, 2, 3
• Prodromal symptoms: lightheadedness, nausea, diaphoresis, pallor, visual blurring 3

Situational Syncope

• Micturition syncope (during or post-urination) 1, 2
• Defecation syncope 1
• Cough or sneeze syncope 1, 4
• Swallowing syncope 1
• Post-exercise syncope 1, 2
• Post-prandial syncope 1, 2

Carotid Sinus Syncope

• Mechanical manipulation of carotid sinuses triggers vasovagal reflex 2
• More common in older adults 2

Important Distinction: Cough syncope differs from classical vasovagal syncope—it involves direct, immediate loss of consciousness following prolonged intensive coughing (often in smokers with lung disease), rather than emotional/orthostatic triggers 4.

Neurogenic Orthostatic Hypotension

This represents autonomic failure where compensatory mechanisms are inadequate:

Primary Autonomic Failure

• Multiple system atrophy 1, 2
• Pure autonomic failure 1, 2
• Parkinson's disease with autonomic failure 1
• Lewy body dementia 1

Secondary Autonomic Failure

• Diabetic neuropathy 1, 2
• Amyloid neuropathy 1, 2
• Uremia 1
• Spinal cord injuries 1

Distinguishing Features: Neurogenic orthostatic hypotension presents with persistent, progressive generalized weakness, fatigue, visual blurring, cognitive slowing, leg buckling, and characteristic "coat hanger" headache—distinct from typical vasovagal prodrome 2.

Non-Syncope Mimics (Critical to Exclude)

These conditions involve loss of consciousness WITHOUT global cerebral hypoperfusion:

With True Loss of Consciousness

• Epileptic seizures 1, 5
• Metabolic disorders: hypoglycemia, hypoxia, hyperventilation with hypocapnia 1
• Intoxication 1
• Vertebrobasilar TIA 1

Without True Loss of Consciousness

• Psychogenic pseudosyncope 1, 5
• Cataplexy 1
• Drop attacks 1
• Falls 1
• Carotid TIA 1

Diagnostic Approach

Initial ECG is Mandatory

• Normal ECG: Low risk for cardiac syncope (with rare exceptions like paroxysmal atrial tachyarrhythmias) 1
• Abnormal ECG: Independent predictor of cardiac syncope and increased mortality—pursue cardiac evaluation 1

Echocardiography Indications

• Low diagnostic yield without clinical/ECG findings suggesting cardiac abnormality 1
• Order when: abnormal physical exam, abnormal ECG, or clinical suspicion of structural disease 1
• Most common incidental finding: mitral valve prolapse (may be coincidental) 1

Autonomic Testing

• Recommended for: Parkinsonism, peripheral neuropathies, progressive autonomic dysfunction, postprandial hypotension, suspected neuropathic POTS 2
• Tilt-table testing with EEG: Can distinguish syncope from pseudosyncope and epilepsy 2

Common Pitfalls

1. Assuming normal blood pressure rules out syncope: Arrhythmias and rapid reflex responses may cause syncope before hypotension is documented 1, 6

2. Missing paroxysmal arrhythmias: Normal baseline ECG doesn't exclude arrhythmic syncope—consider prolonged monitoring if high suspicion 1

3. Over-relying on echocardiography: Low yield without supporting clinical findings; don't use as routine screening 1

4. Confusing neurogenic OH with vasovagal syncope: Look for progressive symptoms, "coat hanger" headache, and absence of typical vasovagal triggers 2, 7

5. Ignoring structural heart disease in elderly: Even with "benign" triggers, underlying cardiac disease dramatically changes risk stratification and management 1, 6