In a 71-year-old woman who fainted after prolonged overhead arm positioning, with a normal emergency department evaluation except an elevated thyroid-stimulating hormone while taking levothyroxine 50 µg daily and daily loratadine, could the elevated TSH be responsible for the syncopal episode or is it solely due to a positional vagal response?

Syncope in a 71-Year-Old Woman: Positional Vagal Episode vs. Elevated TSH

This syncopal episode is almost certainly due to a positional vagal (vasovagal) reflex triggered by prolonged overhead arm positioning, not the mildly elevated TSH of 5.96 mIU/L. The clinical presentation—dizziness followed by loss of consciousness during sustained overhead arm work—is classic for situational reflex syncope, and the benign emergency workup effectively excludes life-threatening cardiac and neurologic causes 1.

Why This Is Vasovagal (Positional) Syncope

The clinical scenario fits perfectly with situational reflex syncope:

• Prolonged overhead arm positioning is a recognized trigger for vasovagal syncope through multiple mechanisms: venous pooling in elevated extremities, increased intrathoracic pressure, and activation of mechanoreceptors that trigger inappropriate vasodilation and bradycardia 1.

• Prodromal dizziness before loss of consciousness is characteristic of vasovagal syncope, which typically presents with warning symptoms (lightheadedness, warmth, visual changes) seconds to minutes before the event 1.

• Complete spontaneous recovery without post-event confusion distinguishes true syncope from seizure or other neurologic causes 1.

• Normal CT scan and benign emergency workup exclude structural cardiac disease, acute ischemia, arrhythmia, and intracranial pathology—the life-threatening causes that must be ruled out first 1.

Why the TSH of 5.96 Is NOT Responsible

A TSH of 5.96 mIU/L represents mild subclinical hypothyroidism and does not cause syncope through direct mechanisms:

• Thyroid-related syncope occurs primarily with severe thyroid dysfunction—either marked hyperthyroidism (causing atrial fibrillation, tachyarrhythmias, or orthostatic intolerance) or profound hypothyroidism (causing bradycardia, pericardial effusion, or severe hemodynamic compromise) 2.

• Subclinical hypothyroidism (elevated TSH with normal free T4) rarely causes cardiovascular symptoms severe enough to produce syncope 2. The TSH of 5.96 suggests her levothyroxine 50 mcg dose is slightly inadequate, but this degree of elevation does not impair cardiac output, cerebral perfusion, or autonomic function sufficiently to cause loss of consciousness 2.

• The temporal relationship is wrong: syncope occurred during a specific positional trigger (overhead arm work), not during rest or routine activity when hypothyroid-related bradycardia or reduced cardiac output would be more likely to manifest 2.

• Hypothyroidism typically causes bradycardia and reduced cardiac output, which would more likely present as exertional fatigue or dyspnea rather than sudden syncope during a specific postural maneuver 2.

Age-Related Considerations in This 71-Year-Old

Elderly patients have unique features that make vasovagal syncope both more common and more atypical in presentation:

• Classic prodromal symptoms may be absent or subtle in older adults, though this patient did report dizziness 1.

• Age-related physiologic changes—reduced baroreceptor sensitivity, diminished autonomic tone, and impaired sodium/water conservation—predispose elderly patients to reflex syncope even with triggers that younger individuals would tolerate 1.

• Polypharmacy is a major contributor: loratadine (Claritin) has mild anticholinergic effects that can impair compensatory tachycardia during vasovagal episodes, potentially lowering the threshold for syncope 1.

• The "fluid on her ear" (likely middle ear effusion from sinusitis) and daily antihistamine use are relevant: antihistamines can cause mild orthostatic hypotension and blunt autonomic responses, compounding age-related vulnerability 1.

What Should Be Done Next

Management should focus on confirming vasovagal syncope and optimizing her thyroid replacement, not attributing the syncope to the TSH:

Immediate Steps:

• Orthostatic vital signs (supine, sitting, standing) should be measured if not already done in the ED to exclude orthostatic hypotension, which is present in 6–33% of elderly syncope patients 1.

• Review the 12-lead ECG for QT prolongation, conduction abnormalities, or ischemic changes that might suggest cardiac syncope 1. A normal ECG strongly supports vasovagal syncope 1.

• Reassure the patient that this was likely a benign reflex response to prolonged arm elevation and does not indicate heart disease or stroke 1.

Thyroid Management:

• Increase levothyroxine to 75 mcg daily and recheck TSH in 6–8 weeks, targeting a TSH of 0.5–2.5 mIU/L for optimal replacement 2. However, emphasize that this adjustment is for long-term thyroid health, not syncope prevention.

• Ensure medication adherence: poor compliance with levothyroxine is common and can lead to fluctuating TSH levels 3.

Syncope Prevention:

• Avoid prolonged overhead arm positioning or take frequent breaks to lower arms and restore venous return 1.

• Increase fluid and salt intake (if not contraindicated by hypertension or heart failure) to expand intravascular volume and reduce vasovagal susceptibility 1, 4.

• Consider discontinuing or reducing loratadine if sinus symptoms allow, as antihistamines can worsen orthostatic tolerance in the elderly 1.

• Teach physical counter-maneuvers: leg crossing, muscle tensing, or squatting at the first sign of dizziness can abort vasovagal episodes 4.

When to Pursue Further Cardiac Workup:

Red-flag features that would mandate cardiology referral or hospitalization include 1, 5:

• Syncope during exertion or while supine/seated (not present here)
• Palpitations immediately before syncope (not reported)
• Family history of sudden cardiac death or inherited arrhythmias (not mentioned)
• Abnormal ECG (stated as normal)
• Known structural heart disease (not present)

None of these high-risk features are present, so outpatient management is appropriate 1.

Common Pitfalls to Avoid

• Do not over-attribute syncope to mild TSH elevation: clinicians often order thyroid tests reflexively in syncope workups, then mistakenly assume causation when TSH is mildly abnormal 2. Thyroid dysfunction severe enough to cause syncope is almost always clinically obvious (profound bradycardia, hypothermia, altered mental status in myxedema; or atrial fibrillation, tremor, weight loss in hyperthyroidism) 2.

• Do not pursue unnecessary neuroimaging: brain CT/MRI in uncomplicated syncope without focal deficits or head trauma yields new diagnoses in <1% of cases 1, 5.

• Do not dismiss vasovagal syncope as trivial: while mortality risk is low, recurrent syncope causes falls, fractures, and significant quality-of-life impairment in the elderly 1, 6. Prevention strategies are essential.

• Do not forget medication review: diuretics, antihypertensives, and anticholinergics are common culprits in elderly syncope 1.