Misconceptions surrounding sodium compounds, particularly the interchangeable use of sodium and sodium chloride (table salt), persist within the medical community, influencing dietary recommendations and patient management especially in heart failure (HF) patients with chronic kidney disease (CKD). This narrative review aims to dissect these misconceptions and discusses the physiological impacts of sodium, chloride, and sodium bicarbonate on cardiovascular (CV) physiology. The conflation of sodium and sodium chloride in dietary recommendations has obscured critical differences in their physiological effects. While sodium chloride is traditionally linked to hypertension, emerging evidence suggests that chloride, rather than sodium, may be the primary driver of hypertension and activation of the renin-angiotensin-aldosterone system. In contrast, sodium bicarbonate, when administered orally, seems to exert minimal effects on blood pressure and plasma volume, offering a promising and safe way for managing HF patients with renal insufficiency. Indeed, the therapeutic benefits of sodium bicarbonate in CKD patients, including preservation of muscle mass, slowing of renal function decline, lowering of all-cause mortality, and improved nutritional status, are quite proven
this underscores its potential utility in patients suffering from both HF and renal insufficiency. Despite concerns about metabolic alkalosis, recent studies suggest that judicious sodium bicarbonate therapy may mitigate major adverse cardiac events without exacerbating HF. This review advocates for a paradigm shift in CV medicine, urging clinicians to discern between sodium chloride and other sodium salts, particularly sodium bicarbonate, in patient care. By elucidating these distinctions, clinicians can tailor dietary recommendations and therapeutic interventions to optimize outcomes for HF patients with CKD and address the multi-faceted complexities of atherosclerotic disease.