Hyponatremia can develop in patients with severe myocardial dysfunction. Issues related to hyponatremia in heart failure will be reviewed here. An overview of the treatment of hyponatremia is presented separately. (See "Overview of the treatment of hyponatremia".)
Like most other causes of hyponatremia, heart failure impairs the ability to excrete ingested water by increasing antidiuretic hormone levels. When cardiac output and systemic blood pressure are reduced, "hypovolemic" hormones, such as renin (with a subsequent increase in angiotensin II formation), antidiuretic hormone (ADH), and norepinephrine, respond [1-3]. Although edematous patients with heart failure have increased plasma and extracellular fluid volumes, the body perceives volume depletion (reduced effective arterial blood volume) since the low cardiac output decreases the pressure perfusing the baroreceptors in the carotid sinus and the renal afferent arteriole.
The degree of neurohumoral activation is generally related to the severity of cardiac dysfunction, as assessed by left ventricular ejection fraction or functional class . The neurohumoral changes limit both sodium and water excretion in an attempt to return perfusion pressure to normal. ADH release directly enhances water reabsorption in the collecting tubules, whereas angiotensin II and norepinephrine limit distal water delivery (and thereby water excretion) by lowering the glomerular filtration rate (due to a marked reduction in renal perfusion) and by increasing proximal sodium and water reabsorption. In addition, both the low cardiac output and high angiotensin II levels are potent stimuli to thirst, leading to enhanced water intake.
PREDICTOR OF ADVERSE PROGNOSIS
Both antidiuretic hormone (ADH) release and the associated reduction in the serum sodium concentration parallel the severity of the heart failure . This relationship has prognostic importance since patient survival is significantly reduced (in comparison to normonatremic patients) once the serum sodium concentration falls below 137 meq/L (figure 1), and even mild hyponatremia is associated with an adverse prognosis following an acute myocardial infarction [4,5]. A similar inverse correlation exists between patient survival and the degree of elevation in serum norepinephrine levels (figure 2). (See "Predictors of survival in heart failure due to systolic dysfunction", section on 'Neurohumoral activation and heart rate'.)
Patients whose serum sodium levels fall below 125 meq/L solely as a result of heart failure usually have near end-stage disease. Patients with heart failure who have this severity of hyponatremia also frequently have hyperkalemia. Distal sodium and water delivery are so low in advanced cardiac disease that potassium excretion (primarily dependent upon distal potassium secretion) falls below the level of intake.