What are the likely causes of presyncope with vomiting?

Causes of Presyncope with Vomiting

Presyncope with vomiting most commonly indicates neurally-mediated (vasovagal) syncope, where vomiting is a recognized prodromal sign of impending cerebral hypoperfusion, though cardiac causes must be urgently excluded given their higher mortality risk.

Primary Mechanism: Neurally-Mediated Syncope

Vomiting is a typical sign of presyncope in vasovagal episodes, appearing alongside other prodromal symptoms including nausea, pallor, sweating, feeling warm/cold, and visual disturbances 1. The underlying pathophysiology involves:

• Decreased cardiac output from reduced venous return to the heart, leading to decreased global cerebral perfusion 1
• Excessive vasodilation with inadequate compensatory vasoconstriction 2, 3
• Vasovagal syncope accounts for 21.2% of all syncopal episodes and is generally benign, though injury risk remains significant 1

Critical High-Risk Features Requiring Urgent Cardiac Evaluation

You must immediately assess for cardiac causes, which carry the highest morbidity and mortality risk 2. Red flags include:

• Age >60 years 1, 2
• Male gender 1
• Known cardiac disease (ischemic heart disease, structural abnormalities, previous arrhythmias, reduced ventricular function) 1, 2
• Brief or absent prodrome before symptoms 1
• Syncope during exertion or in supine position 1, 2
• Palpitations preceding the episode 2
• Family history of sudden cardiac death or inheritable conditions 1, 2

Specific Etiologies to Consider

Neurally-Mediated (Reflex) Causes

• Classical vasovagal syncope: Triggered by emotional stress, pain, prolonged standing, fear, or distressful stimuli 1, 4
• Situational syncope: Associated with specific triggers including micturition, defecation, cough, swallowing, or gastrointestinal stimulation 1, 2
• Rare vagovagal reflex: Vomiting itself can trigger complete heart block through esophageal distension activating a vagovagal reflex, causing ventricular asystole 5

Orthostatic Hypotension (9.4% of cases)

• Drug-induced: Diuretics, beta-blockers, calcium antagonists, ACE inhibitors, nitrates, antipsychotics, tricyclic antidepressants 1, 2
• Volume depletion: Hemorrhage, diarrhea, Addison's disease 2
• Autonomic failure: Diabetic neuropathy, Parkinson's disease, multiple system atrophy 2, 4

Cardiac Arrhythmias (Highest Mortality Risk)

• Bradyarrhythmias: Sinus node dysfunction, high-grade AV block, Mobitz type II block 2
• Tachyarrhythmias: Ventricular tachycardia, inherited syndromes (long QT, Brugada), drug-induced proarrhythmias 2

Structural Cardiac Disease

• Obstructive lesions: Aortic stenosis, hypertrophic obstructive cardiomyopathy 2
• Acute conditions: Myocardial infarction/ischemia, aortic dissection, pulmonary embolism, cardiac tamponade 2

Immediate Clinical Assessment Algorithm

Every patient requires these three components 1:

1. Detailed history focusing on:

   • Positional relationship (standing vs. supine) 1
   • Specific triggers (meals, exertion, emotional stress) 1
   • Prodromal symptoms duration and character 1
   • Medication review, especially in elderly 2

2. Physical examination:

   • Orthostatic vital signs: Measure blood pressure and heart rate lying, sitting, immediately upon standing, and after 3 minutes upright 1
   • Cardiac examination for murmurs, gallops, structural disease 1
   • Basic neurological examination for focal deficits 1

3. 12-lead ECG (Class I recommendation):

   • Can identify arrhythmogenic substrates (Wolff-Parkinson-White, Brugada, long QT, hypertrophic cardiomyopathy) 1
   • Detects conduction abnormalities, ischemia, or prior infarction 1

Critical Pitfalls to Avoid

• Do not dismiss presyncope as less serious than syncope—both conditions share similar prognoses and require identical evaluation 2, 3
• Avoid routine head CT in uncomplicated presentations without head trauma or focal neurological deficits (yield <1%) 2, 3
• Do not overlook cardiac causes in elderly patients, where age-related physiological changes (reduced baroreceptor response, autonomic dysfunction, polypharmacy) increase vulnerability 2
• Recognize that seizure-like activity can occur with cardiac syncope, including myoclonic jerks and brief automatisms, which may be mistaken for primary neurological events 2

Management Based on Risk Stratification

Low-risk patients (young, no cardiac disease, clear vasovagal trigger, normal ECG):

• Reassurance and education 6, 7
• Physical counterpressure maneuvers: Leg crossing, muscle tensing, squatting when prodrome occurs (Class 2a recommendation) 1
• Maintain safe position (sitting or lying down) when symptoms begin 1
• Increase fluid and salt intake 4, 8

High-risk patients (any cardiac red flags, abnormal ECG):

• Hospital admission for urgent evaluation 6
• Continuous cardiac monitoring 6
• Echocardiography to assess structural disease 6
• Consider electrophysiology consultation for arrhythmia evaluation 6