Hyponatremia pathophysiology

Sterns RH, Narins RG. Hypernatremia and hyponatremia Pathophysiology, diagnosis, and therapy. In Androgue HJ, ed. Contemporary Management in Critical Care, Vol. 1, No. 2. Acid-Base and Electrolyte Disorders. New York, Churchill Livingstone, 1991 161-191. 

The potent antidiuretic hormone AVP orchestrates the regulation of free water absorption, body fluid osmolality, cell contraction, blood volume, and blood pressure through stimulation of three G-protein-coupled receptor subtypes Vi-vascular types a and b, V2-renal, and V3-pituitary. Increased AVP secretion is the trademark of several pathophysiological disorders, including heart failure, impaired renal function, liver cirrhosis, and SIADH. As a consequence, these patients experience excess water retention or inadequate free-water excretion, which results in the dilution of sodium concentrations, frequently manifesting as clinical hyponatremia (serum sodium concentration <135mmol/L). This electrolyte imbalance increases mortality rates by 60-fold. Selective antagonism of the AVP V2 receptor promotes water... 

HYPONATREMIA (SERUM SODIUM LESS THAN 135 MEQ/L) Pathophysiology... 

In patients with a low plasma osmolality (hypotonicity), the most important step in the diagnostic evalnation of hyponatremia is the clinical assessment of the extraceUnlar flnid volume. Categorization of patients with hypotonic hyponatremia into one of three gronps (decreased, increased, or clinically normal ECF volnme) is crucial in order to identify the pathophysiologic mechanisms responsible for the hyponatremia and thereby propose an appropriate treatment regimen (Fig. 49-2). 

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