Acute Hemodynamic Decompensation Following Routine Phlebotomy in a Patient with Chronic Volume Dysregulation: A Five-Week Longitudinal Provocation Sequence

A 48-year-old male (DOB 7/5/1969) with a documented history of chronic volume dysregulation and suspected endocrine axis disruption underwent routine whole blood donation as a self-initiated provocation test. Within 24-48 hours, the patient experienced a transient hypercortisolemic state (subjective mania), followed by acute vestibular failure on day three, persistent nausea and orthostatic symptoms over the subsequent four weeks, and a near-syncopal collapse on day 34 triggered by THC-induced vasodilation. Throughout the collapse event, the patient maintained full consciousness despite documented blood pressure of 90/54 mmHg post-saline resuscitation. Serial laboratory evaluation revealed prerenal azotemia (BUN 27 mg/dL), borderline hypokalemia (K 3.5 mEq/L), maximally concentrated urine (SG 1.033), venous alkalosis (pH 7.44), complete suppression of eosinophils and basophils, and urine sodium of 203 mmol/L (massive renal sodium wasting despite volume depletion), while standard cardiac and structural workups returned negative. Longitudinal endocrine data spanning 2010 to 2026 demonstrate stable cortisol (10.3-13.2 mcg/dL) against declining aldosterone (6.5 to 4.0 ng/dL) with volatile intermediate values (1.5 ng/dL two weeks prior to the crisis), suggesting selective adrenal output preservation independent of the renin-angiotensin system. This case documents a complete provocation-response sequence with timed clinical and laboratory endpoints in a patient whose hemodynamic architecture operates outside standard physiological parameters.[A note from The Architect: All PDF’s of these labs and more are at jimcraddock.com]https://www.jimcraddock.com/