Persistent hyperchloremia with chronically low CO₂ consistent with non–anion gap metabolic acidosis (NAGMA) was observed despite preserved renal function in a patient later found to have heart failure with reduced ejection fraction (HFrEF). The constellation of electrolyte abnormalities, autonomic instability, endocrine disruption, and gastrointestinal dysfunction appeared across multiple medical specialties yet was not interpreted as a single physiologic process. This paper proposes that a subset of HFrEF cases may represent a reversible systems-level phenotype termed Terrain-Induced Functional Cardiomyopathy (TIFC). In this model, cardiac suppression arises not from structural myocardial injury but from coordinated regulatory collapse along a Vertical Terrain Axis involving bile signaling, RAAS interpretation, chloride buffering patterns, metabolic voltage stability, and autonomic regulation. The framework suggests that physiologic collapse may unfold sequentially across interconnected regulatory layers. Bile-mediated signaling through FXR and TGR5 receptors influences nitric oxide availability, vascular tone, and neurohormonal signaling pathways that interact with renal RAAS interpretation and downstream electrolyte handling. Under sustained metabolic and hydration stress, these mechanisms may favor chloride retention relative to bicarbonate, producing a hyperchloremic NAGMA terrain state. Mitochondrial energetic suppression and autonomic dysregulation may follow, ultimately expressed as reduced cardiac ejection fraction despite structurally intact myocardium. Unlike structural cardiomyopathies, TIFC demonstrates potential reversibility when upstream regulatory coordination is restored, including normalization of bile flow, electrolyte balance, acid–base buffering, and metabolic stability. This paper represents the clinical cardiovascular expression layer of the Lantern of Sulfur Concept A triad. Companion papers describe the regulatory timing architecture (circadian layer) and the metabolic load layer (KICO model), together forming a systems framework linking physiologic timing, metabolic rhythm, electrolyte terrain signals, and downstream cardiovascular expression. Recognition of chloride-dominant electrolyte terrain patterns and hydration–metabolic regulatory instability may allow earlier identification of reversible functional cardiomyopathy states before structural cardiac damage occurs.
Beth Ann Martell (Wed,) studied this question.