Water, Na, K Balance PDF

Water, Sodium and Potassium Introduction Water balance: -60% of body weight is provided by water. -Total body water is distributed between 2 main compartments: a)65% intracellular fluid (ICF). b)35% extracellular fluid (EFC). Water movement in fluid compartments: Water is not actively tran...

Water, Sodium and Potassium Introduction Water balance: -60% of body weight is provided by water. -Total body water is distributed between 2 main compartments: a)65% intracellular fluid (ICF). b)35% extracellular fluid (EFC). Water movement in fluid compartments: Water is not actively transported in the body. It is, in general, freely permeable through the ICF and ECF and its distribution is determined by the osmotic contents of these compartments. 1 Under normal circumstances, the amounts of water taken into the body and lost from it are equal over a period of time. 2 Water is obtained from diet and oxidative metabolism and is lost through the kidneys, skin, lungs and gut. About 170 L of water is filtered by the kidneys every 24 h, and almost all of this is reabsorbed. The minimum volume of urine necessary for normal excretion of waste products is about 500 mL/24 h but, as a result of obligatory losses by other routes, the minimum daily water intake necessary for the maintenance of water balance is approximately 1100 mL. This increases if losses are abnormally large, for example with excessive sweating or diarrhoea. Water intake is usually considerably greater than this minimum requirement, but the excess is easily excreted through the kidneys.Water and ECF osmolality Changes in body water content independent of the amount of solute will alter the osmolality. Any loss of water from the ECF, such as occurs with water deprivation, will increase its osmolality and result in movement of water from the ICF to the ECF. However, a slight increase in ECF osmolality will still occur, stimulating the hypothalamic thirst centre, causing thirst and thus promoting a desire to drink, and stimulation of the hypothalamic 3  osmoreceptors, which causes the release of vasopressin (ADH). Constituents of fluid compartments in the body 1. Electrolytes: in the ionic form such as sodium and potassium (expressed as m Eq/L). 2. Non-electrolytes: such as glucose, urea, and creatinine -Their concentrations in IC and EC compartments vary. -Water freely travels from one compartment to another. -Water crosses the cell membrane in both directions depending on the concentrations of solid particles (solutes) on each side. -Water moves from areas of lower solute concentration to that of higher solute concentration, this process is called Osmosis. 4 Sodium -Na is the most important ion in regulating water balance. Sodium distribution The body of an adult man contains approximately 4000 mmol of sodium, 70% of which is freely exchangeable, the remainder being complexed in bone. The majority of the exchangeable sodium is extracellular. ECF sodium concentration is 135-145 mmol/L(serum level), while that of the ICF is only 4-10 mmol/L. Most cell membranes are relatively impermeable to sodium, but some leakage into cells occurs and the gradient is maintained by active pumping of sodium from the ICF to the ECF by NaKATPase. Sodium functions: 1.Membrane potentials. 2.Accounts for 90-95% of osmolality of ECF. 3.Na+ - K+ pump. Exchanges intracellular Na+ for extra cellular K+. 5  Creates gradient for transports of other solutes (glucose). Generates heat. 4.NaHCO3 has a major role in buffering pH. Sodium-Homeostasis a) Excretion of dietary excess. -0.5 g/day needed, typical diet has 3 to 7 g/day. b) Aldosterone – “salt retaining hormone”. -Hypernatremia / hypokalemia inhibitsits release. c)ADHincreases blood Na+ levels. -Kidneys reabsorp more water (without retaining more Na+) d)ANP (atrial natriuretic peptide) from stretched arteries. -Kidneys excrete more Na+ and H2O, thus decreasesblood pressure. e) Other-estrogen retains water during pregnancy. -Progesterone has diuretic effect. 6 Sodium – Imbalance: Hypernatremia: -Plasma sodium > 145 mEq/L -From IV saline, drowning, acute and chronic renal Failure. -Water retension, hypertension and eodema. Hyponatremia: -Plasma sodium < 13 mEq/L as in vomiting, diarhoea and excess sweating. -Result of excess body water, quickly corrected by excretion of excess water. Potassium Normal plasma level 3.5-5 mEq/LPotassium distribution Potassium is the predominant intracellular cation. 90% of the total body potassium is free and therefore exchangeable, while the remainder is bound in red blood cells, bone and brain tissue. Potassium function: 1.Most abundant cation of ICF. 2.Determines intracellular osmolality. 3.Membrane potentials (with sodium). 4.Na+ - K+ pump. 7 Potassium homeostasis: 90% of K+ in glomerular filtrate is reabsorbed by PCT. Aldosterone stimulates renal secretion of K+. Potassium Imbalances: 1.Hyperkalemia: effects depends on rate of electrolytes. -If concentration rises quickly (crush injury) the sudden increase in extracellular K+ makes nerve and muscle cells abnormally excitable. -Slow onset, nerve and muscle cells become less excitable Hypokalemia: -Sweating, chronic vomiting or diarrhoea, laxatives. -Nerve and muscle cells less excitable. -Muscle weakness, loss of muscle tone, arrthymias. 8 Osmolality: Is a term used to define total solute concentration expressed as milliosmol per liter (mosm/L). -Disturbance of electrolyte contents of ICF or ECF results in clinical signs and symptoms. -This should be recognized and corrected otherwise will result in altered homeostasis, and death. Fluid balance: a) Regulation of water intake: Water intake is controlled by sensation of thirst and output by anti- diuretic hormone (ADH). Dehydration: mean - Blood volume and pressure. -blood osmolality. -→ Loss of water from ECF increases osmolality. This will cause: -Movement of water from ICF → ECF. -Stimulates hypothalamus thirst center which promotes the desire of drink. -In states of water deficiency → plasma osmolality  →causing a sensation of thirst and stimulating arginine vasopressin (AVP) → both mediated by hypothalamic osmoreceptors. 9 In turn, AVP promotes water reabsorption in the distal nephron. In case of increased water intake → suppresses thirst → and reduces → AVP secretion → leading to a brisk diuresis. Thirst mechanisms: a) Stimulation of thirst center (in hypothalamus). b) Angiotensin II is produced in response to  Bp. c) ADH: produced in response to  blood osmolality. d) Hypothalamic osmoreceptors: signal in response to  ECF osmolality. Regulators of vasopressin release: I. Osmotic control: Hypothalamic osmoreceptors sensitive for small changes in osmolality as small as 1%. II. Baroreceptor: - In the left atrium and great vessels on the left side of the heart. - Decreased blood volume/pressure stimulates the release of ADH. - Baroreceptor is less sensitive than the osmoreceptors detect 8-10% change in volume or pressure. 10 Factors affecting ADH secretion Stimulated by Inhibited by High osmolality Low ECF osmolality Low blood volume High blood volume Low blood pressure High blood pressure Stress including pain Alcohol Regulation of output: -Only control over water output is through variations in urine volume. -By controlling Na+ reabsorption as withNa+reabsorpion or excretion, water follows. -By action of ADH →ADH secretion (as well as thirst center) stimulated by hypothalamic osmoreceptors in response to dehydration Disorders of water balance: Fluid deficiency: Volume depletion (hypovolemia): -Total body water , osmolality normal. -Hemorrhage, severe burns, chronic vomiting or diarrhea. Dehydration: -Total body water , osmolality rise. 11 -Lack of drinking water, diabetes, profuse sweating, diuretics. -Gastroenteritis -High metabolic rate demands high urine excretion, kidneys cannot concentrate urine effectively. -Affects all fluid compartments. -Most serious effects: circulatory shock, neurological dysfunction, infant mortality. Fluid Excess: -Both Na+ and water retained, ECF isotonic. -Aldosterone hypersecretion. Hypotonic hydration: -More water than Na+ retained or ingested, ECF hypotonic can cause cellular swelling. -Most serious effects are pulmonary and cerebral edema. Fluid sequestration: -Excess fluid in a particular location. → Most common form: edema. -Pleural effusions. → Several liters of fluid may accumulate in plural membrane as in lung infections. 12 Decreased excreation: a)Renal failure. b)Increase ADH secrtion -Prevents urinary excretion of water. -Results in state of water excess -Low plasma osmolality, low plasma Na+. c)Some drugs (e.g. cortisol). SUMMARY Sodium, potassium and water homoeostasis are closely linked. Sodium is the principal extracellular cation and the amount of sodium in the body is the major determinant of ECF volume. Potassium is the major intracellular cation Sodium and potassium are transported actively in the body; water moves passively in response to changes in the solute contents of the body's fluid compartments Sodium excretion is primarily controlled by aldosterone, a hormone secreted in response to a decrease in ECF volume that causes sodium retention and loss of potassium Water excretion is controlled by vasopressin (antidiuretic hormone). This promotes water retention and is secreted in 13 response to an increase in ECF osmolality and a decrease in ECF volume Potassium excretion is regulated in part by aldosterone, but also depends on extracellular hydrogen ion concentration and sodium and water excretion Disturbances of either water or sodium homoeostasis can produce characteristic clinical and biochemical features, but combined disturbances are common and the features may then be less clear- cut Changes in plasma sodium concentration can be due to changes in the amounts of extracellular sodium or water or both. Hyponatraemia is common; it is sometimes an appropriate physiological response to disease. Hypernatraemia is less common than hyponatraemia, and usually is related to a decrease in body water Plasma potassium concentration is a poor guide to the body's overall potassium status. Depletion is not always associated with hypokalaemia, nor is hypokalaemia always due to potassium depletion; similar considerations apply to potassium excess and hyperkalaemia Hypokalaemia is most frequently a result of excessive gastrointestinal or renal loss of potassium and may be exacerbated by a poor intake. It can also be a consequence of increased cellular 14 uptake of potassium from the plasma. It can cause skeletal and smooth muscle weakness and impairment of myocardial contractility and renal concentrating ability. It also potentiates digoxin toxicity Hyperkalaemia is most frequently due to decreased renal excretion or to loss of potassium from cells; hyperkalaemia is often iatrogenic, occurring as a result of drug treatment or inappropriate potassium administration. Spurious hyperkalaemia, due to release of potassium from cells in vitro, is common. Hyperkalaemia can cause cardiac arrest: this can occur in the absence of any warning clinical symptoms or signs. 15