Fluid, Electrolyte, and Acid-Base Balance: Introduction to Body Fluids Essay

   Fluid Compartments Water occupies two main fluid compartments Intracellular fluid (ICF) – about two thirds by volume, contained in cells Extracellular fluid (ECF) – consists of two major subdivisions Plasma – the fluid portion of the blood Interstitial fluid (IF) – fluid in spaces between cells Other ECF – lymph, cerebrospinal fluid, eye humors, synovial fluid, serous fluid, and gastrointestinal secretions Extracellular and Intracellular Fluids Water is the universal solvent Solutes are broadly classified into: Electrolytes – inorganic salts, all acids and bases, and some proteins Electrolytes determine the chemical and physical reactions of fluids Electrolytes have greater osmotic power than nonelectrolytes Water moves according to osmotic gradients Nonelectrolytes – examples include glucose, lipids, creatinine, and urea Each fluid compartment of the body has a distinctive pattern of electrolytes Extracellular fluids are similar (except for high protein content of plasma) Sodium is the chief cation Chloride is the major anion Intracellular fluids have low sodium and chloride Potassium is the chief cation Phosphate is the chief anion Proteins, phospholipids, cholesterol, and neutral fats account for: 90% of the mass of solutes in plasma 60% of the mass of solutes in interstitial fluid 97% of the mass of solutes in the intracellular compartment Fluid Movement Among Compartments Compartmental exchange is regulated by osmotic and hydrostatic pressures Net leakage of fluid from the blood is picked up by lymphatic vessels and returned to the bloodstream Exchanges between interstitial and intracellular fluids are complex due to the selective permeability of the cellular membranes Two-way water flow is substantial Ion fluxes are restricted and move selectively by active transport Nutrients, respiratory gases, and wastes move unidirectionally Plasma is the only fluid that circulates throughout the body and links external and internal environments Osmolalities of all body fluids are equal; changes in solute concentrations are quickly followed by osmotic changes Water Balance and ECF Osmolality To remain properly hydrated, water intake must equal water output Water intake sources Ingested fluid (60%) and solid food (30%) Metabolic water or water of oxidation (10%) Water output Urine (60%) and feces (4%) Insensible losses (28%), sweat (8%) Increases in plasma osmolality trigger thirst and release of antidiuretic hormone (ADH) Regulation of Water – Homeostaisis Intake – Hypothalmic Thirst Center Thirst is quenched as soon as we begin to drink water Feedback signals that inhibit the thirst centers include: Moistening of the mucosa of the mouth and throat Activation of stomach and intestinal stretch receptors Influence and Regulation of ADH Water reabsorption in collecting ducts is proportional to ADH release Low ADH levels produce dilute urine and reduced volume of body fluids High ADH levels produce concentrated urine Hypothalamic osmoreceptors trigger or inhibit ADH release Factors that specifically trigger ADH release include prolonged fever; excessive sweating, vomiting, or diarrhea; severe blood loss; and traumatic burns Disorders of Water Balance: Dehydration Water loss exceeds water intake and the body is in negative fluid balance Causes include: hemorrhage, severe burns, prolonged vomiting or diarrhea, profuse sweating, water deprivation, and diuretic abuse Signs and symptoms: cottonmouth, thirst, dry flushed skin, and oliguria Prolonged dehydration may lead to weight loss, fever, mental confusion Other consequences include hypovolemic shock and loss of electrolytes Hypotonic Hydration Renal insufficiency or an extraordinary amount of water ingested quickly can lead to cellular overhydration, or water intoxication ECF is diluted – sodium content is normal but excess water is present The resulting hyponatremia promotes net osmosis into tissue cells, causing swelling These events must be quickly reversed to prevent severe metabolic disturbances, particularly in neurons Edema. Atypical accumulation of fluid in the interstitial space, leading to tissue swelling Caused by anything that increases flow of fluids out of the bloodstream or hinders their return. Factors that accelerate fluid loss  include: Increased blood pressure, capillary permeability Incompetent venous valves, localized blood vessel blockage Congestive heart failure, hypertension, high blood volume Hindered fluid return usually reflects an imbalance in colloid osmotic pressures Hypoproteinemia – low levels of plasma proteins Forces fluids out of capillary beds at the arterial ends Fluids fail to return at the venous ends Results from protein malnutrition, liver disease, or glomerulonephritis Blocked (or surgically removed) lymph vessels: Cause leaked proteins to accumulate in interstitial fluid Exert increasing colloid osmotic pressure, which draws fluid from the blood Interstitial fluid accumulation results in low blood pressure and severely impaired circulation Sodium in Fluid and Electrolyte Balance Sodium holds a central position in fluid and electrolyte balance Sodium salts: Account for 90-95% of all solutes in the ECF Contribute 280 mOsm of the total 300 mOsm ECF solute concentration Sodium is the single most abundant cation in the ECF Sodium is the only cation exerting significant osmotic pressure The role of sodium in controlling ECF volume and water distribution in the body is a result of: Sodium being the only cation to exert significant osmotic pressure Sodium ions leaking into cells and being pumped out against their electrochemical gradient Sodium concentration in the ECF normally remains stable Changes in plasma sodium levels affect: Plasma volume, blood pressure ICF and interstitial fluid volumes Renal acid-base control mechanisms are coupled to sodium ion transport Regulation of Sodium Balance: Aldosterone The renin-angiotensin mechanism triggers the release of aldosterone This is mediated by juxtaglomerular apparatus, which releases renin in response to: Sympathetic nervous system stimulation Decreased filtrate osmolality Decreased stretch due to decreased blood pressure Renin catalyzes the production of angiotensin II, which prompts aldosterone release Adrenal cortical cells are directly stimulated to release aldosterone by elevated K+ levels in the ECF Aldosterone brings about its effects (diminished urine output and increased blood volume) slowly Cardiovascular System Baroreceptors Baroreceptors alert the brain of increases in blood volume (hence increased blood pressure) Sympathetic nervous system impulses to the kidneys decline Afferent arterioles dilate Glomerular filtration rate rises Sodium and water output increase This phenomenon, called pressure diuresis, decreases blood pressure Drops in systemic blood pressure lead to opposite actions and systemic blood pressure increases Since sodium ion concentration determines fluid volume, baroreceptors can be viewed as â€Å"sodium receptors† Atrial Natriuretic Peptide (ANP) Reduces blood pressure and blood volume by inhibiting: Events that promote vasoconstriction Na+ and water retention Is released in the heart atria as a response to stretch (elevated blood pressure) Has potent diuretic and natriuretic effects Promotes excretion of sodium and water Inhibits angiotensin II production Influence of Other Hormones on Sodium Balance Estrogens: Enhance NaCl reabsorption by renal tubules May cause water retention during menstrual cycles Are responsible for edema during pregnancy Progesterone: Decreases sodium reabsorption Acts as a diuretic, promoting sodium and water loss Glucocorticoids – enhance reabsorption of sodium and promote edema Regulation of Potassium Balance Relative ICF-ECF potassium ion concentration affects a cell’s resting membrane potential Excessive ECF potassium decreases membrane potential Too little K+ causes hyperpolarization and nonresponsiveness Hyperkalemia and hypokalemia can: Disrupt electrical conduction in the heart Lead to sudden death Hydrogen ions shift in and out of cells Leads to corresponding shifts in potassium in the opposite direction Interferes with activity of excitable cells Influence of Aldosterone Aldosterone stimulates potassium ion secretion by principal cells In cortical collecting ducts, for each Na+ reabsorbed, a K+ is secreted Increased K+ in the ECF around the adrenal cortex causes: Release of aldosterone –>Potassium secretion Potassium controls its own ECF concentration via feedback regulation of aldosterone release Regulation of Calcium Ionic calcium in ECF is important for: Blood clotting Cell membrane permeability Secretory behavior Hypocalcemia: Increases excitability, causes muscle tetany Hypercalcemia: inhibits neurons and muscle cells; cause heart arrhythmias Calcium balance is controlled by parathyroid hormone and calcitonin PTH promotes increase in calcium levels by targeting: Bones – PTH activates osteoclasts to break down bone matrix Small intestine – PTH enhances intestinal absorption of calcium Kidneys – PTH enhances calcium reabsorption and decreases phosphate reabsorption Calcium reabsorption and phosphate excretion go hand in hand Influence of Calcitonin Released in response to rising blood calcium levels Calcitonin is a PTH antagonist, but its contribution to calcium and phosphate homeostasis is minor to negligible Acid Base Balance Introduction to Acids and Bases Strong acids – all their H+ is dissociated completely in water Weak acids – dissociate partially in water and are efficient at preventing pH changes Strong bases – dissociate easily in water and quickly tie up H+ Weak bases – accept H+ more slowly (e.g., HCO3 ¯ and NH3) Normal pH of body fluids Arterial blood is 7.4 Venous blood and interstitial fluid is 7.35 Intracellular fluid is 7.0 Alkalosis or alkalemia – arterial blood pH rises above 7.45 Acidosis or acidemia – arterial pH drops below 7.35 (physiological acidosis) Sources of Hydrogen Ions – Most hydrogen ions originate from cellular metabolism Breakdown of phosphorus-containing proteins releases phosphoric acid into the ECF Anaerobic respiration of glucose produces lactic acid Fat metabolism yields organic acids and ketone bodies Transporting carbon dioxide as bicarbonate releases hydrogen ions Hydrogen Ion Regulation Concentration of hydrogen ions is regulated sequentially by: Chemical buffer systems – act within seconds Physiological buffer systems The respiratory center in the brain stem – acts within 1-3 minutes Renal mechanisms – require hours to days to effect pH changes Chemical Buffer Systems Bicarbonate Buffer System A mixture of carbonic acid (H2CO3) and its salt, sodium bicarbonate (NaHCO3) (potassium or magnesium bicarbonates work as well) If strong acid is added: Hydrogen ions released combine with the bicarbonate ions and form carbonic acid (a weak acid) The pH of the solution decreases only slightly If strong base is added: It reacts with the carbonic acid to form sodium bicarbonate (a weak base) The pH of the solution rises only slightly This system is the only important ECF buffer Phosphate Buffer System Nearly identical to the bicarbonate system Its components are: Sodium salts of dihydrogen phosphate (H2PO4 ¯), a weak acid Monohydrogen phosphate (HPO42 ¯), a weak base This system is an effective buffer in urine and intracellular fluid Protein Buffer System Plasma and intracellular proteins are the body’s most plentiful and powerful buffers Some amino acids of proteins have: Free organic acid groups (weak acids) Groups that act as weak bases (e.g., amino groups) Amphoteric molecules are protein molecules that can function as both a weak acid and a weak base Physiological Buffer Systems Respiratory Buffer System The respiratory system regulation of acid-base balance is a physiological buffering system There is a reversible equilibrium between: Dissolved carbon dioxide and water Carbonic acid and the hydrogen and bicarbonate ions CO2 + H2O –> H2CO3 –> H+ + HCO3 ¯ During carbon dioxide unloading, hydrogen ions are incorporated into water When hypercapnia or rising plasma H+ occurs: Deeper and more rapid breathing expels more carbon dioxide Hydrogen ion concentration is reduced Alkalosis causes slower, more shallow breathing, causing H+ to increase Respiratory system impairment causes acid-base imbalance (respiratory acidosis or respiratory alkalosis) Renal Mechanisms of Acid-Base Balance Introduction Chemical buffers can tie up excess acids or bases, but they cannot eliminate them from the body The lungs can eliminate carbonic acid by eliminating carbon dioxide Only the kidneys can rid the body of metabolic acids (phosphoric, uric, and lactic acids and ketones) and prevent metabolic acidosis The ultimate acid-base regulatory organs are the kidneys The most important renal mechanisms for regulating acid-base balance are: Conserving (reabsorbing) or generating new bicarbonate ions Excreting bicarbonate ions Losing a bicarbonate ion is the same as gaining a hydrogen ion; reabsorbing a bicarbonate ion is the same as losing a hydrogen ion Hydrogen ion secretion occurs in the PCT Hydrogen ions come from the dissociation of carbonic acid Reabsorption of Bicarbonate CO2 combines with water in tubule cells, forming H2CO3 H2CO3 splits into H+ and HCO3- For each H+ secreted, a Na+ and a HCO3- are reabsorbed by the PCT cells Secreted H+ form H2CO3; thus, HCO3- disappears from filtrate at the same rate that it enters the peritubular capillary blood H2CO3 formed in filtrate dissociates to release CO2 + H2 CO2 then diffuses into tubule cells, where it acts to trigger further H+ secretion Hydrogen Ion Excretion Dietary H+ must be counteracted by generating new HCO3- The excreted H+ must bind to buffers in the urine (phosphate buffer system) Intercalated cells actively secrete H+ into urine, which is buffered and excreted HCO3- generated is: Moved into the interstitial space via a cotransport system Passively moved into the peritubular capillary blood In response to acidosis: Kidneys generate HCO3-and add them to the blood An equal amount of H+ are added to the urine Ammonium Ion (NH4+) Excretion This method uses NH4+ produced by the metabolism of glutamine in PCT cells Each glutamine metabolized produces two ammonium ions and two bicarbonate ions HCO3- moves to the blood and ammonium ions are excreted in urine Respiratory Acidosis and Alkalosis Result from failure of the respiratory system to balance pH PCO2 is the single most important indicator of respiratory inadequacy PCO2 levels – normal PCO2 fluctuates between 35 and 45 mm Hg Values above 45 mm Hg signal respiratory acidosis Values below 35 mm Hg indicate respiratory alkalosis Respiratory acidosis is the most common cause of acid-base imbalance Occurs when a person breathes shallowly, or gas exchange is hampered by diseases such as pneumonia, cystic fibrosis, or emphysema Respiratory alkalosis is a common result of hyperventilation Metabolic Acidosis All pH imbalances except those caused by abnormal blood carbon dioxide levels Metabolic acid-base imbalance – bicarbonate ion levels above or below normal (22-26 mEq/L) Metabolic acidosis is second most common cause of acid-base imbalance Typical causes are ingestion of too much alcohol and excessive loss of bicarbonate ions Other causes include accumulation of lactic acid, shock, ketosis in diabetic crisis, starvation, and kidney failure Metabolic Alkalosis Rising blood pH and bicarbonate levels indicate metabolic alkalosis Typical causes are: Vomiting of the acid contents of the stomach Intake of excess base (e.g., from antacids) Constipation, in which excessive bicarbonate is reabsorbed Respiratory and Renal Compensations Acid-base imbalance due to inadequacy of a physiological buffer system is compensated for by the other system The respiratory system will attempt to correct metabolic acid-base imbalances The kidneys will work to correct imbalances caused by respiratory disease Respiratory Compenstaion In metabolic acidosis: The rate and depth of breathing are elevated Blood pH is below 7.35 and bicarbonate level is low As carbon dioxide is eliminated by the respiratory system, PCO2 falls below normal In metabolic alkalosis: Compensation exhibits slow, shallow breathing, allowing carbon dioxide to accumulate in the blood Correction is revealed by: High pH (over 7.45) and elevated bicarbonate ion levels RisingPCO2 Renal Compensation To correct respiratory acid-base imbalance, renal mechanisms are stepped up Acidosis has high PCO2 and high bicarbonate levels The high PCO2 s the cause of acidosis The high bicarbonate levels indicate the kidneys are retaining bicarbonate to offset the acidosis Alkalosis has Low PCO2 and high pH The kidneys eliminate bicarbonate from the body by failing to reclaim it or by actively secreting it