Case Presentation: A 37-year-old incarcerated woman presented with recurrent dizziness, presyncope, and intermittent chest tightness. She had persistent orthostatic hypotension (systolic 70–100 mmHg; MAP often < 65 mmHg) and bradycardia (30s–50s). Serial ECGs showed sinus bradycardia without atrioventricular block; chest radiography was normal; transthoracic echocardiography showed preserved ejection fraction and no significant valvular disease. Initial labs: sodium 135 mmol/L, potassium 3.9 mmol/L, creatinine 0.60 mg/dL. Thyroid testing fluctuated during admission: free T4 0.59–0.60 ng/dL with TSH 16.67 µIU/mL, then 1.44 µIU/mL, then 16.67 µIU/mL. Cosyntropin testing confirmed adrenal insufficiency (baseline cortisol 2.5 µg/dL; only increased to 8.9 µg/dL). ACTH was low, indicating central adrenal insufficiency. Pituitary MRI with sellar protocol was normal. Orthostatic vitals were repeatedly positive; heart rate rose appropriately with ambulation. A dopamine infusion increased heart rate but not MAP, arguing against a primary cardiac cause. Electrophysiology deemed her chronotropically competent and advised against pacemaker. Management included a brief stint on pressors initially, stress-dose hydrocortisone, midodrine up-titrated to 15 mg three times daily, and a short course of fludrocortisone initially. Because hypotension began after starting lithium and fluphenazine ~3 months earlier, psychiatry discontinued both and initiated aripiprazole 10 mg daily; buprenorphine-naloxone was continued. Given ongoing orthostasis despite steroid replacement, AL amyloidosis was considered; urine immunofixation detected faint lambda Bence Jones protein. She stabilized, ambulated with minimal dizziness, and was discharged with outpatient light-chain evaluation and cardiac MRI planned.
Discussion: This vignette shows why hospitalist-led care matters when rare endocrine and cardiac processes overlap. At the bedside, the practical question was heart, medications, or hormones. Three pivotal inpatient decisions redirected care: (1) cosyntropin testing with low ACTH confirmed central adrenal insufficiency as the driver of catecholamine-refractory hypotension; (2) demonstration of chronotropic competence and absent MAP response to dopamine argued against conduction disease and avoided an unnecessary pacemaker; (3) “swinging” thyroid studies (high TSH, then normal TSH, then high TSH) prompted an infiltrative workup—urine immunofixation revealed a faint lambda light-chain (Bence Jones) signal, raising early AL amyloidosis as a unifying autonomic process. Hospitalists integrated telemetry and orthostatics, deprescribed bradycardia-provoking agents, optimized midodrine and glucocorticoids, and coordinated cardiology/electrophysiology, and psychiatry—core competencies of hospital medicine.
Conclusions: In persistent orthostatic hypotension with sinus bradycardia, hospitalist-directed confirmation of central adrenal insufficiency and proof of chronotropic competence can prevent invasive pacing and refocus therapy on endocrine/autonomic causes. Volatile thyroid indices should trigger infiltrative evaluation; even a faint monoclonal light chain warrants amyloidosis workup. This case underscores hospitalists’ test-driven, multidisciplinary management to resolve refractory hypotension and enable safe transitions of care.