Fluid electolyte and acid-base balance A.pptx
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Fluid, Electrolyte and Acid-Base Balance Objectives • List factors that affect body water content • List routes by which water enters and leaves body • Describe water regulation and role of hormones • Name body fluids and identify locations • Distinguish between electrolytes and non-electrolytes •...
Fluid, Electrolyte and Acid-Base Balance Objectives • List factors that affect body water content • List routes by which water enters and leaves body • Describe water regulation and role of hormones • Name body fluids and identify locations • Distinguish between electrolytes and non-electrolytes • Describe regulation of selected electrolytes • List the 3 major chemical buffers systems and briefly describe how the function. Body Water Content • Infants have low body fat, low bone mass, and are 73% or more water • Total water content declines throughout life • Healthy males are about 60% water; healthy females are around 50% • This difference reflects females’: • Higher body fat • Smaller amount of skeletal muscle • In old age, only about 45% of body weight is water 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 Fluid Compartments Figure 26.1 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 Balance and ECF Osmolality • Water output • Urine (60%) and feces (4%) • Insensible losses (28%), sweat (8%) • Increases in plasma osmolality trigger thirst and release of antidiuretic hormone (ADH) Water Intake and Output Figure 26.4 Regulation of Water Intake • The hypothalamic thirst center is stimulated: • By a decline in plasma volume of 10%–15% • By increases in plasma osmolality of 1–2% • Via baroreceptor input, angiotensin II, and other stimuli Regulation of Water Intake • 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 Regulation of Water Intake: Thirst Mechanism Figure 26.5 Regulation of Water Output • Obligatory water losses include: • Insensible water losses from lungs and skin • Water that accompanies undigested food residues in feces • Obligatory water loss reflects the fact that: • Kidneys excrete 900-1200 mOsm of solutes to maintain blood homeostasis • Urine solutes must be flushed out of the body in water 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 Mechanisms and Consequences of ADH Release Figure 26.6 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, and mental confusion • Other consequences include hypovolemic shock and loss of electrolytes Disorders of Water Balance: Dehydration 1 Excessive loss of H2O from ECF 2 ECF osmotic pressure rises 3 Cells lose H2O to ECF by osmosis; cells shrink (a) Mechanism of dehydration Figure 26.7a Disorders of Water Balance: 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 Disorders of Water Balance: Hypotonic Hydration 1 Excessive H2O enters the ECF 2 ECF osmotic pressure falls 3 H2O moves into cells by osmosis; cells swell (b) Mechanism of hypotonic hydration Figure 26.7b Disorders of Water Balance: 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 Electrolyte Balance • Electrolytes are salts, acids, and bases, but electrolyte balance usually refers only to salt balance • Salts are important for: • • • • Neuromuscular excitability Secretory activity Membrane permeability Controlling fluid movements • Salts enter the body by ingestion and are lost via perspiration, feces, and urine Electrolyte Composition of Body Fluids Figure 26.2 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 • Sodium is the single most abundant cation in the ECF • Sodium is the only cation exerting significant osmotic pressure Sodium in Fluid and Electrolyte Balance • 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 Sodium in Fluid and Electrolyte Balance • 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 • Sodium reabsorption • 65% of sodium in filtrate is reabsorbed in the proximal tubules • 25% is reclaimed in the loops of Henle • When aldosterone levels are high, all remaining Na+ is actively reabsorbed • Water follows sodium if tubule permeability has been increased with ADH Regulation of Sodium Balance: Aldosterone • The renin-angiotensin mechanism triggers the release of aldosterone • This is mediated by the 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 Regulation of Sodium Balance: Aldosterone • 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 Regulation of Sodium Balance: Aldosterone Figure 26.8 Maintenance of Blood Pressure Homeostasis Figure 26.9 Mechanisms and Consequences of ANP Release Figure 26.10 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 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 Regulation of Potassium Balance • 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 Regulatory Site: Cortical Collecting Ducts • Less than 15% of filtered K+ is lost to urine regardless of need • K+ balance is controlled in the cortical collecting ducts by changing the amount of potassium secreted into filtrate • Excessive K+ is excreted over basal levels by cortical collecting ducts • When K+ levels are low, the amount of secretion and excretion is kept to a minimum • Type A intercalated cells can reabsorb some K+ left in the filtrate Influence of Plasma Potassium Concentration • High K+ content of ECF favors principal cells to secrete K+ • Low K+ or accelerated K+ loss depresses its secretion by the collecting ducts 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 Regulation of Calcium • Hypercalcemia: • Inhibits neurons and muscle cells • May cause heart arrhythmias • Calcium balance is controlled by parathyroid hormone (PTH) and calcitonin Regulation of Calcium and Phosphate • 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 Regulation of Calcium and Phosphate • Filtered phosphate is actively reabsorbed in the proximal tubules • In the absence of PTH, phosphate reabsorption is regulated by its transport maximum and excesses are excreted in urine • High or normal ECF calcium levels inhibit PTH secretion • Release of calcium from bone is inhibited • Larger amounts of calcium are lost in feces and urine • More phosphate is retained Regulation of Anions • Chloride is the major anion accompanying sodium in the ECF • 99% of chloride is reabsorbed under normal pH conditions • When acidosis occurs, fewer chloride ions are reabsorbed • Other anions have transport maximums and excesses are excreted in urine Acid-Base Balance • 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 • 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 • 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) Chemical Buffer Systems • One or two molecules that act to resist pH changes when strong acid or base is added • Three major chemical buffer systems • Bicarbonate buffer system • Phosphate buffer system • Protein buffer system • Any drifts in pH are resisted by the entire chemical buffering system 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 Bicarbonate Buffer System • 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 • 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¯ Physiological Buffer Systems • 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 • 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 Renal Mechanisms of Acid-Base Balance • 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 Renal Mechanisms of Acid-Base Balance • Hydrogen ion secretion occurs in the PCT and in type A intercalated cells • Hydrogen ions come from the dissociation of carbonic acid Reabsorption of Bicarbonate • Carbon dioxide combines with water in tubule cells, forming carbonic acid • Carbonic acid splits into hydrogen ions and bicarbonate ions • For each hydrogen ion secreted, a sodium ion and a bicarbonate ion are reabsorbed by the PCT cells • Secreted hydrogen ions form carbonic acid; thus, bicarbonate disappears from filtrate at the same rate that it enters the peritubular capillary blood • Carbonic acid of Bicarbonate Reabsorption formed in filtrate dissociates to release carbon dioxide and water • Carbon dioxide then diffuses into tubule cells, where it acts to trigger further hydrogen ion secretion Figure 26.12 Generating New Bicarbonate Ions • Two mechanisms carried out by type A intercalated cells generate new bicarbonate ions • Both involve renal excretion of acid via secretion and excretion of hydrogen ions or ammonium ions (NH4+) • Dietary hydrogen ions must be counteracted Hydrogen Ion Excretion by generating new bicarbonate • The excreted hydrogen ions must bind to buffers in the urine (phosphate buffer system) • Intercalated cells actively secrete hydrogen ions into urine, which is buffered and excreted • Bicarbonate generated is: • Moved into the interstitial space via a cotransport system • Passively moved into the peritubular capillary blood • In response to Excretion Hydrogen Ion acidosis: • Kidneys generate bicarbonate ions and add them to the blood • An equal amount of hydrogen ions are added to the urine Figure 26.13 Ammonium Ion Excretion • This method uses ammonium ions produced by the metabolism of glutamine in PCT cells • Each glutamine metabolized produces two ammonium ions and two bicarbonate ions • Bicarbonate moves to the blood and ammonium ions are excreted in urine Ammonium Ion Excretion Figure 26.14 Bicarbonate Ion Secretion • When the body is in alkalosis, type B intercalated cells: • Exhibit bicarbonate ion secretion • Reclaim hydrogen ions and acidify the blood • The mechanism is the opposite of type A intercalated cells and the bicarbonate ion reabsorption process • Even during alkalosis, the nephrons and collecting ducts excrete fewer bicarbonate ions than they conserve 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 and Alkalosis • Respiratory acidosis is the most common cause of acidbase 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 the 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 acidbase imbalances • The kidneys will work to correct imbalances caused by respiratory disease Respiratory Compensation • 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, P CO2 falls below normal • In respiratory acidosis, the respiratory rate is often depressed and is the immediate cause of the acidosis Respiratory Compensation • 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 • Rising PCO2 Renal Compensation • To correct respiratory acid-base imbalance, renal mechanisms are stepped up • Acidosis has high PCO2 and high bicarbonate levels • The high PCO2 is the cause of acidosis • The high bicarbonate levels indicate the kidneys are retaining bicarbonate to offset the acidosis • Alkalosis has Low P and high pH Renal Compensation CO2 • The kidneys eliminate bicarbonate from the body by failing to reclaim it or by actively secreting it PLAY InterActive Physiology®: Fluid, Electrolyte, and Acid/Base Balance: Acid/Base Homeostasis Developmental Aspects • Water content of the body is greatest at birth (70-80%) and declines until adulthood, when it is about 58% • At puberty, sexual differences in body water content arise as males develop greater muscle mass • Homeostatic mechanisms slow down with age • Elders may be unresponsive to thirst clues and are at risk of dehydration • The very young and the very old are the most frequent victims of fluid, acid-base, and electrolyte imbalances Problems with Fluid, Electrolyte, and Acid-Base Balance • Occur in the young, reflecting: • Low residual lung volume • High rate of fluid intake and output • High metabolic rate yielding more metabolic wastes • High rate of insensible water loss • Inefficiency of kidneys in infants
