Disturbances of Plasma Sodium (2) PDF

Dr Damian Griffin Consultant Chemical Pathologist Basis for investigating disturbances of plasma sodium  Plasma sodium is primarily a surrogate marker of plasma osmolality.  Are the key regulatory systems working as expected?  Osmoregulation  Effective circulating volume regulation  The...

Dr Damian Griffin Consultant Chemical Pathologist Basis for investigating disturbances of plasma sodium  Plasma sodium is primarily a surrogate marker of plasma osmolality.  Are the key regulatory systems working as expected?  Osmoregulation  Effective circulating volume regulation  The correlation of plasma sodium & osmolality and the regulatory responses to disturbances in plasma sodium usually enable us to elucidate the cause of the disturbance Sodium & Osmolality  Our bodies primarily regulate osmolality, not sodium  It would therefore make sense for us to monitor plasma osmolality rather than plasma sodium  However we don’t routinely measure osmolality, as analytical methods for osmolality are not easily automated  Sodium is the major extracellular contributor to osmolality & under most circumstances it correlates with osmolality.  Sodium is relatively easy to measure, so we use it as a surrogate marker for plasma osmolality  In the assessment of hyponatraemia it is important to be on the look out for situations in which the normal correlation between sodium and osmolality is disturbed Osmoregulation  This regulatory system is governed by osmoreceptors in the hypothalamus that respond to changes in plasma osmolality  The responses to hyperosmolality are:  Thirst which regulates free water intake  Secretion of the antidiuretic hormone, arginine vasopressin, via the posterior pituitary gland, which regulates water excretion by the kidneys.  It is important to note that even though osmoregulation is a response to changes in plasma osmolality, these changes are almost entirely mediated by changes in water balance, not salt balance!  ↑Plasma osmolality ↑Osmoreceptor stimulation Thirst ↑ADH secretion Drink water ↑Urine osmolality ↓Plasma osmolality Osmoregulation Effective Circulating Volume (ECV) Regulation  Effective circulating volume (ECV) is not a quantitatively measurable entity but refers to the rate of perfusion of the capillary circulation.  ECV is maintained by varying vascular resistance, cardiac output, as well as renal sodium and water excretion  The body senses changes in ECV through volume receptors (aka baroreceptors, stretch receptors) in the cardiopulmonary circulation, the carotid sinuses and the aortic arch, and the afferent glomerular arterioles in the kidney.  The response to changes in ECV is primarily through the sympathetic nervous system, angiotensin II generation, regulation of renal Na+ excretion.  ↓Effective circulating volume ↑Baroreceptor stimulation ↑Sympathetic tone ↑Renin secretion ↑Angiotensin II formation Venous constriction Arterial constriction ↑Cardiac contractility + ↑Heart rate ↑Aldosterone secretion ↑Venous return ↑Vascular resistance ↑Tubular Na+ reabsorption ↑Cardiac output ↑Blood pressure ECV Regulation ↑Effective circulating volume Hypernatraemia  Hypernatraemia represents both extracellular and intracellular hyperosmolality.  The increase in plasma osmolality induced by the rise in plasma Na+ creates an osmotic gradient that results in water movement out of the cells and into the extracellular fluid.  Hypernatraemia is almost exclusively due to an impairment of the osmoregulatory system  However, understanding the effective circulating volume regulatory system help us interpret what is happening Case 1  60 year old woman, living Plasma alone, found unconscious. Na+ 167 mmol/L (135-145) She had a stroke one or two K+ 3.5 mmol/L (3.5-5.0) days earlier. On admission: Cl- 125 mmol/L (98-108)  Pulse rate 80/min, blood HCO3- 24 mmol/L (23-33) pressure 140/80, considered Urea 22.5 mmol/L (3.0-8.0) to be dehydrated Creat 220 µmol/L (60-120) Osmol 356 mmol/L (280-295) Urine Na+