Fundamentals of Anatomy & Physiology

Fundamentals of Anatomy & Physiology
Eleventh Edition Chapter 27 Fluid, Electrolyte, and Acid-Base Balance Lecture Presentation by Deborah A. Hutchinson Seattle University

27-1 Fluid, Electrolyte, and Acid-Base Balance
Water Makes up 99 percent of fluid volume outside cells Extracellular fluid (ECF) Essential ingredient of cytosol inside cells Intracellular fluid (ICF) All cellular operations rely on water As diffusion medium for gases, nutrients, and wastes

27-1 Fluid, Electrolyte, Acid-Base Balance
Volumes, solute concentrations, and pH of ECF and ICF Stabilized by three interrelated processes Fluid balance Electrolyte balance Acid-base balance

Fluid balance Daily balance between Amount of water gained Amount of water lost to environment Involves regulating content and distribution of body water in ECF and ICF Digestive system Primary source of water gains Urinary system Primary route of water loss

Electrolyte balance Electrolytes Ions released through dissociation of inorganic compounds Can conduct electrical current in solution When gains and losses for every electrolyte are in balance Primarily involves balancing rates of absorption across digestive tract with rates of loss at kidneys

Precisely balances production and loss of hydrogen ions (H+) Body generates acids during normal metabolism Reduce pH Kidneys Secrete H+ into urine Generate buffers that enter bloodstream Lungs Affect pH through elimination of carbon dioxide

27-2 Fluid Compartments Body water content Mostly in ICF
Water accounts for roughly 60 percent of adult male body weight 50 percent of adult female body weight

27-2 Fluid Compartments Fluid compartments of ECF and ICF
Intracellular fluid (ICF) Cytosol inside cells Extracellular fluid (ECF) Primarily, interstitial fluid of peripheral tissues and plasma of circulating blood

27-2 Fluid Compartments Extracellular fluid (ECF) Minor components
Lymph Cerebrospinal fluid (CSF) Synovial fluid Serous fluids (pleural, pericardial, and peritoneal) Aqueous humor Perilymph Endolymph

27-2 Fluid Compartments ECF and ICF
Called fluid compartments because they behave as distinct entities Maintain different ionic compositions Ions ECF Sodium, chloride, and bicarbonate ions ICF Potassium, magnesium, and phosphate ions Negatively charged proteins

Figure 27–2 Cations and Anions in Body Fluids (Part 1 of 3).
INTRACELLULAR FLUID KEY 200 Cations Na+ HCO3– Cl– Na+ K+ 150 Ca2+ Milliequivalents per liter (mEq/L) HPO42– Mg2+ K+ 100 Anions HCO3– SO42– Cl– HPO42– 50 SO42– Proteins Organic acid Mg2+ Proteins Cations Anions

PLASMA 200 KEY Cations Na+ K+ 150 HCO3– Ca2+ Milliequivalents per liter (mEq/L) Mg2+ 100 Anions HCO3– Na+ Cl– Cl– HPO42– 50 HPO42– SO42– Org. acid Organic acid K+ Proteins Ca2+ Proteins Cations Anions

INTERSTITIAL FLUID KEY 200 Cations Na+ K+ 150 Ca2+ Milliequivalents per liter (mEq/L) HCO3– Mg2+ 100 Anions HCO3– Na+ Cl– Cl– HPO42– 50 SO42– Organic acid HPO42– SO42– K+ Proteins Cations Anions

27-2 Fluid Compartments Osmotic concentrations of ICF and ECF
Identical Osmosis across plasma membranes eliminates minor differences Ion exchange Between ICF and ECF occurs across selectively permeable plasma membranes by Osmosis Diffusion Carrier-mediated transport

27-2 Fluid Compartments Exchanges among subdivisions of ECF
Occur primarily across endothelial lining of capillaries Also from interstitial spaces to plasma Via lymphatic vessels that drain into venous system

27-2 Fluid Compartments Solute content of ECF
Varies regionally in types and amounts of Electrolytes Proteins Nutrients Wastes

27-2 Fluid Compartments Regulation of fluids and electrolytes
All homeostatic mechanisms that monitor and adjust body fluid composition respond to changes in ECF, not ICF No receptors directly monitor fluid or electrolyte balance Cells cannot move water by active transport Body’s water or electrolyte content will rise if dietary gains exceed environmental losses, and will fall if losses exceed gains

27-2 Fluid Compartments Primary hormones that regulate fluid and electrolyte balance Antidiuretic hormone Aldosterone Natriuretic peptides

27-2 Fluid Compartments Antidiuretic hormone (ADH)
Stimulates water conservation at kidneys Reducing urinary water loss Concentrating urine Stimulates hypothalamic thirst center Promoting fluid intake

27-2 Fluid Compartments ADH production and release
Osmoreceptors in hypothalamus Monitor osmotic concentration of ECF Axons of osmoreceptor neurons in hypothalamus Release ADH near fenestrated capillaries in posterior lobe of pituitary gland Higher osmotic concentration increases ADH release

27-2 Fluid Compartments Aldosterone
Secreted by adrenal cortex in response to Rising K+ or falling Na+ levels in blood Activation of renin-angiotensin-aldosterone system Determines rate of Na+ reabsorption and K+ loss in kidneys High aldosterone plasma concentration Causes kidneys to conserve Na+ Also stimulates water retention “Water follows salt”

27-2 Fluid Compartments Natriuretic peptides
Atrial natriuretic peptide (ANP) B-type natriuretic peptide (BNP) Released by cardiac muscle cells In response to abnormal stretching of heart walls Reduce thirst Block release of ADH and aldosterone Cause diuresis (fluid loss by kidneys) Lower blood pressure and plasma volume

27-3 Fluid Balance Fluid balance
When amounts of water gained and lost each day are equal Body’s water content and Na+ concentration of ECF are inversely correlated

27-3 Fluid Balance Fluid gains and losses Water gains
About 2500 mL/day required to balance water losses Drinking (1200 mL) Eating (1000 mL) Metabolic generation (300 mL) Metabolic generation of water within cells Results from oxidative phosphorylation in mitochondria

27-3 Fluid Balance Fluid gains and losses Water losses
About 2500 mL each day Urine Feces Insensible perspiration Sensible perspiration (sweat) varies with activities Can cause significant water loss (4 L/hr) Fever can increase water losses

27-3 Fluid Balance Water can move between ECF and ICF
Normally in osmotic equilibrium No large-scale circulation between them

27-3 Fluid Balance Fluid movement within ECF Water circulates freely
Net hydrostatic pressure Pushes water out of plasma Into interstitial fluid Net colloid osmotic pressure Draws water out of interstitial fluid Into plasma Interaction between opposing forces Results in continuous filtration of fluid

27-3 Fluid Balance Fluid movement within ECF
ECF fluid volume is redistributed From lymphatic vessels to venous circulation ECF volume 80 percent is in interstitial fluid and minor fluid compartments 20 percent in plasma

27-3 Fluid Balance Edema (swelling)
Movement of abnormal amounts of water from plasma into interstitial fluid Lymphedema Edema caused by blockage of lymphatic drainage

27-3 Fluid Balance Fluid shifts
Rapid water movements between ECF and ICF In response to an osmotic gradient If osmotic concentration of ECF increases Fluid becomes hypertonic to ICF Water moves from cells to ECF If osmotic concentration of ECF decreases Fluid becomes hypotonic to ICF Water moves from ECF into cells

27-3 Fluid Balance Fluid shifts
ICF volume is much greater than ECF volume ICF acts as water reserve Prevents large osmotic changes in ECF

27-3 Fluid Balance Dehydration (water depletion)
Develops when water losses are greater than gains If water is lost, but electrolytes retained ECF osmotic concentration rises Water moves from ICF to ECF Because of large volume, net change in ICF is small

27-3 Fluid Balance Severe water loss May result from
Excessive perspiration Inadequate water consumption Repeated vomiting Diarrhea Homeostatic responses Physiological mechanisms (ADH and renin secretion) Behavioral changes (increasing fluid intake)

27-3 Fluid Balance Distribution of water gains
If water is gained, but electrolytes are not ECF volume increases ECF becomes hypotonic to ICF Fluid shifts from ECF to ICF May result in hyperhydration (water excess) Occurs when excess water shifts into ICF Distorting cells Changing solute concentrations around enzymes Disrupting normal cell functions

27-3 Fluid Balance Causes of hyperhydration
Ingestion of a large volume of water Injection of hypotonic solution into bloodstream Inability to eliminate excess water in urine Chronic renal failure Heart failure Cirrhosis Endocrine disorders Excessive ADH production

27-3 Fluid Balance Signs of hyperhydration
Abnormally low Na+ concentrations (hyponatremia) Effects on CNS function (water intoxication)

27-4 Electrolyte Balance Electrolyte balance
When gains and losses are equal for each electrolyte in body Total electrolyte concentrations directly affect water balance Concentrations of individual electrolytes affect cell functions

27-4 Electrolyte Balance Sodium Dominant cation in ECF
Sodium salts provide 90 percent of ECF osmotic concentration Sodium chloride (NaCl) Sodium bicarbonate (NaHCO3)

27-4 Electrolyte Balance General rules of electrolyte balance
Most common problems with electrolyte balance are caused by imbalance between gains and losses of Na+ Problems with K+ balance are less common but more dangerous than Na+ imbalance

27-4 Electrolyte Balance Sodium balance
Total amount of Na+ in ECF represents a balance between two factors Na+ uptake across digestive epithelium Na+ excretion in urine and perspiration

27-4 Electrolyte Balance Sodium balance Typical Na+ gains and losses
48–144 mEq (1.1–3.3 g) per day If gains exceed losses Total Na+ content of ECF rises If losses exceed gains Na+ content of ECF declines

27-4 Electrolyte Balance Sodium balance and ECF volume
Na+ regulatory mechanism changes ECF volume Keeps Na+ concentration fairly stable When Na+ gains exceed losses Plasma Na+ concentration increases temporarily Fluid exits ICF in fluid shift, increasing ECF volume Normal concentration of Na+ is maintained When Na+ losses exceed gains ECF volume and osmotic concentration decrease Water loss at kidneys regains osmotic balance

27-4 Electrolyte Balance Large changes in ECF volume
Corrected by homeostatic mechanisms that regulate blood volume and pressure If ECF volume rises, blood volume goes up If ECF volume drops, blood volume goes down A rise in blood volume elevates blood pressure A drop in blood volume lowers blood pressure ECF volume can be monitored indirectly as baroreceptors monitor blood pressure

27-4 Electrolyte Balance Disorders of sodium balance Hyponatremia
Body water content rises (hyperhydration) Na+ concentration of ECF <135 mEq/L Hypernatremia Body water content declines (dehydration) Na+ concentration of ECF >145 mEq/L

27-4 Electrolyte Balance If ECF volume is inadequate
Blood volume and blood pressure decline Renin-angiotensin-aldosterone system is activated Water and Na+ losses are reduced Water and Na+ gains are increased ECF volume increases

27-4 Electrolyte Balance If plasma volume is too large
Venous return increases Stimulating release of natriuretic peptides Reduce thirst Block secretion of ADH and aldosterone Salt and water loss at kidneys increases ECF volume decreases

27-4 Electrolyte Balance Potassium balance
98 percent of potassium in body is in ICF Cells expend energy to recover K+ that diffused from cytoplasm into ECF Concentration of K+ in ECF is a balance between Rate of gain across digestive epithelium Rate of loss in urine

27-4 Electrolyte Balance Potassium losses in urine
Regulated by activities of ion pumps Along distal convoluted tubule and collecting system Na+ from tubular fluid are exchanged for K+ (typically) in peritubular fluid Limited to amount gained by absorption across digestive epithelium About 50–150 mEq (1.9–5.8 g) per day

27-4 Electrolyte Balance Factors affecting rate of K+ secretion into urine Changes in K+ concentration of ECF Changes in pH Aldosterone levels

27-4 Electrolyte Balance Changes in K+ concentration of ECF
Higher K+ concentration in ECF leads to higher rate of secretion Changes in pH Low pH of ECF lowers pH of peritubular fluid H+ rather than K+ are exchanged for Na+ in tubular fluid Rate of K+ secretion declines

27-4 Electrolyte Balance Aldosterone levels Affect K+ loss in urine
Ion pumps sensitive to aldosterone reabsorb Na+ from tubular fluid in exchange for K+ High plasma K+ concentration also stimulates aldosterone secretion directly

27-4 Electrolyte Balance Disorders of K+ imbalance Hypokalemia
Deficiency of K+ in bloodstream Hyperkalemia Elevated level of K+ in bloodstream

Figure 27–7 Major Factors Involved in Disturbances of Potassium Ion Balance.
When the blood concentration of K+ falls below 2 mEq/L, extensive muscular weakness develops, followed by eventual paralysis. Severe hypokalemia is potentially lethal due to its effects on the heart. High K+ concentration in the blood produces an equally dangerous condition known as hyperkalemia. Severe hyperkalemia occurs when the K+ concentration exceeds 7 mEq/L, which results in cardiac arrhythmias. Normal potassium range in blood: (3.5–5.0 mEq/L) Factors Promoting Hypokalemia Factors Promoting Hyperkalemia Several diuretics can produce hypokalemia by increasing the volume of urine produced. The endocrine disorder called aldosteronism, characterized by excessive aldosterone secretion, results in hypokalemia by overstimulating Na+ retention and K+ loss. Chronically low blood pH promotes hyperkalemia by interfering with K+ excretion by the kidneys. Kidney failure due to damage or disease will prevent normal K+ secretion and thereby produce hyperkalemia. Several drugs promote diuresis by blocking Na+ reabsorption by the kidneys. When Na+ reabsorption slows down, so does K+ secretion, and hyperkalemia can result.

27-4 Electrolyte Balance Calcium balance
Calcium is most abundant mineral in body A typical person has 1–2 kg 99 percent of which is deposited in skeleton Calcium ions (Ca2+) function In muscular and neural activities In blood clotting As cofactors for enzymatic reactions As second messengers

27-4 Electrolyte Balance Hormones and calcium homeostasis
Parathyroid hormone (PTH) and calcitriol Raise Ca2+ concentrations in ECF Calcitonin Opposes PTH and calcitriol

27-4 Electrolyte Balance Ca2+ gains Absorption at digestive tract
Reabsorption in kidneys Both stimulated by PTH and calcitriol Ca2+ losses In bile, urine, or feces Very small (0.8–1.2 g/day) Represents about 0.03 percent of calcium reserve in skeleton

27-4 Electrolyte Balance Hypercalcemia
Exists if Ca2+ concentration in ECF is >5.3 mEq/L Usually caused by hyperparathyroidism Resulting from oversecretion of PTH Other causes Malignant cancers (breast, lung, kidney, and bone marrow) Excessive calcium or vitamin D supplementation

27-4 Electrolyte Balance Hypocalcemia
Exists if Ca2+ concentration in ECF is <4.3 mEq/L Usually caused by Hypoparathyroidism (undersecretion of PTH) Vitamin D deficiency Chronic renal failure

27-4 Electrolyte Balance Magnesium balance
Adult body contains about 29 g of magnesium About 60 percent is deposited in skeleton Magnesium ions (Mg2+) in body fluids are primarily in ICF Required as a cofactor for enzymatic reactions Phosphorylation of glucose Use of ATP by contracting muscle fibers Effectively reabsorbed by kidneys Daily dietary requirement is about 24–32 mEq

27-4 Electrolyte Balance Phosphate balance
Phosphate ions (PO43–) are required for bone mineralization About 740 g are bound in mineral salts of skeleton In ICF, PO43– are required for formation of high-energy compounds, activation of enzymes, and synthesis of nucleic acids Plasma concentration is usually 1.8–3.0 mEq/L PO43– are reabsorbed in kidneys Daily urinary and fecal losses total 30–45 mEq

27-4 Electrolyte Balance Chloride balance
Chloride ions are most abundant anions in ECF Plasma concentration is 100–108 mEq/L ICF concentrations are usually low (3 mEq/L) Cl–are absorbed across digestive tract with Na+ And reabsorbed with Na+ by carrier proteins along renal tubules Daily loss is only 48–146 mEq (1.7–5.1 g)

27-5 Acid-Base Balance pH A measure of acidity or alkalinity of a solution pH of body fluids depends on dissolved Acids Bases Salts pH of body fluids is altered by addition of acids or bases pH of ECF Narrowly limited, usually 7.35–7.45

Table 27–3 A Review of Important Terms Relating to Acid-Base Balance

27-5 Acid-Base Balance Acidosis
Physiological state resulting from abnormally low blood pH Acidemia is when blood pH <7.35 Alkalosis Physiological state resulting from abnormally high blood pH Alkalemia is when blood pH >7.45

27-5 Acid-Base Balance Acidosis and alkalosis
Affect virtually all body systems Particularly nervous and cardiovascular systems Both are dangerous But acidosis is more common Because normal cellular activities generate acids Acid-base balance Control of pH Homeostatic process of great physiological and clinical significance

27-5 Acid-Base Balance Types of acids in body Fixed acids
Metabolic acids Volatile acids

27-5 Acid-Base Balance Fixed acids Acids that do not leave solution
Once produced they remain in body fluids Until eliminated by kidneys Sulfuric acid and phosphoric acid Most important fixed acids in body Generated during catabolism of Amino acids Phospholipids Nucleic acids

27-5 Acid-Base Balance Metabolic acids
Participants in, or by-products of, cellular metabolism Pyruvic acid Lactic acid Ketone bodies Metabolized rapidly under normal conditions Significant accumulations do not occur

27-5 Acid-Base Balance Volatile acids
Can leave body by entering atmosphere at lungs Carbonic acid (H2CO3) breaks down into carbon dioxide and water CO2 diffuses from bloodstream into alveoli

27-5 Acid-Base Balance Carbonic anhydrase
Enzyme that catalyzes formation of carbonic acid from carbon dioxide and water Found in Cytoplasm of red blood cells Liver and kidney cells Parietal cells of stomach Many other cells

27-5 Acid-Base Balance CO2 and pH
Most CO2 in solution converts to carbonic acid Most carbonic acid dissociates into Hydrogen ions (H+) Bicarbonate ions (HCO3–) Partial pressure of CO2 (PCO2) The most important factor affecting blood pH

27-5 Acid-Base Balance PCO2 and pH are inversely related
When CO2 levels rise H+ and HCO3– are released pH decreases At alveoli CO2 diffuses into atmosphere H+ and HCO3– in alveolar capillaries decrease Blood pH rises

27-5 Acid-Base Balance Mechanisms of pH control
To maintain homeostasis, the body balances Gains and losses of hydrogen ions

27-5 Acid-Base Balance Hydrogen ions (H+) Gained At digestive tract
Through cellular metabolic activities Eliminated At kidneys At lungs Must be neutralized to avoid tissue damage Acids produced in normal metabolic activity Temporarily neutralized by buffers in body fluids

27-5 Acid-Base Balance Acids and bases may be strong or weak
Strong acids and strong bases Dissociate completely in solution Example: hydrochloric acid (HCl) Weak acids or weak bases Do not dissociate completely in solution Some molecules remain intact Weak acid releases fewer H+ than does a strong acid, and thus has less effect on pH of solution

27-5 Acid-Base Balance Carbonic acid Weak acid In ECF at normal pH
Equilibrium state exists: H2CO3 ↔ H+ + HCO3–

27-5 Acid-Base Balance Buffers
Dissolved compounds that stabilize pH of solution By adding or removing H+ Weak acids Can donate H+ Weak bases Can absorb H+

27-5 Acid-Base Balance Buffer system Consists of a combination of
A weak acid An anion released by its dissociation Anion functions as a weak base In solution, molecules of the weak acid exist in equilibrium with its dissociation products

27-5 Acid-Base Balance Three major buffer systems
Phosphate buffer system Protein buffer systems Carbonic acid–bicarbonate buffer system

Figure 27–10 Buffer Systems in Body Fluids.
occur in Intracellular fluid (ICF) Extracellular fluid (ECF) a Phosphate Buffer System b Protein Buffer Systems c Carbonic Acid– Bicarbonate Buffer System Protein buffer systems contribute to the regulation of pH in the ECF and ICF. These buffer systems interact extensively with the other two buffer systems. The phosphate buffer system has an important role in buffering the pH of the ICF and of urine. The carbonic acid– bicarbonate buffer system is most important in the ECF. Hemoglobin buffer system (RBCs only) Amino acid buffers (all proteins) Plasma protein buffers

27-5 Acid-Base Balance Phosphate buffer system
Consists of H2PO4– (a weak acid) and its anion (HPO42–) Cells contain a weak base (Na2HPO4) Provides additional HPO42– for this buffer system Important in buffering pH of ICF and urine

27-5 Acid-Base Balance Protein buffer systems Rely on amino acids
Respond to pH changes by accepting or releasing H+ Important in ECF and ICF If pH rises Carboxyl group of amino acid dissociates Releasing a hydrogen ion, acting as weak acid Carboxyl group becomes carboxylate ion

27-5 Acid-Base Balance Protein buffer systems At normal pH (7.35–7.45)
Carboxyl groups of most amino acids have already given up their H+ If pH decreases Carboxylate ion and amino group act as weak bases Accepting H+ Forming carboxyl group and amino ion

27-5 Acid-Base Balance Protein buffer systems
Carboxyl and amino groups in peptide bonds cannot function as buffers Most buffering capacity of proteins is provided by R groups of amino acids

27-5 Acid-Base Balance Hemoglobin buffer system
CO2 in plasma rapidly diffuses into red blood cells And is converted to carbonic acid As carbonic acid dissociates Bicarbonate ions diffuse into plasma In exchange for chloride ions (chloride shift) Hydrogen ions are buffered by hemoglobin molecules

27-5 Acid-Base Balance Hemoglobin buffer system
The only intracellular buffer system with an immediate effect on pH of ECF Helps prevent major changes in pH when plasma PCO2 is rising or falling

27-5 Acid-Base Balance Carbonic acid–bicarbonate buffer system
Carbon dioxide Constantly generated by body cells Most is converted to carbonic acid This buffer system involves carbonic acid and its dissociation products H+ and bicarbonate ions Prevents changes in pH caused by metabolic acids and fixed acids in ECF

27-5 Acid-Base Balance Limitations of carbonic acid–bicarbonate buffer system Cannot protect ECF from changes in pH that result from increased or decreased levels of CO2 Functions only when respiratory system and respiratory control centers are working normally Ability to buffer acids is limited by availability of bicarbonate ions

27-5 Acid-Base Balance Bicarbonate ion shortage is rare because
Body fluids contain large reserve of sodium bicarbonate Called bicarbonate reserve Additional HCO3– can be generated by kidneys

27-5 Acid-Base Balance Limitations of buffer systems
Provide only temporary solution to acid-base imbalance Do not eliminate H+ Supply of buffer molecules is limited

27-5 Acid-Base Balance Regulation of acid-base balance
To preserve homeostasis, captured H+ must be Permanently tied up in water molecules through CO2 removal at lungs Removed from body fluids by secretion at kidneys Requires balancing H+ gains and losses To maintain body pH within narrow limits, buffer systems coordinate with Respiratory mechanisms Renal mechanisms

27-5 Acid-Base Balance Respiratory and renal mechanisms
Support buffer systems by Secreting or absorbing H+ Controlling excretion of acids and bases Generating additional buffers

27-5 Acid-Base Balance Respiratory compensation
Change in respiratory rate Helps stabilize pH of ECF Occurs whenever body pH moves outside normal limits Directly affects carbonic acid–bicarbonate buffer system

27-5 Acid-Base Balance Respiratory compensation
Increasing or decreasing rate of respiration alters pH by lowering or raising PCO2 When PCO2 rises pH falls Addition of CO2 drives buffer system to right When PCO2 falls pH rises Removal of CO2 drives buffer system to left

27-5 Acid-Base Balance Renal compensation
Change in rates of H+ and HCO3– secretion or reabsorption by kidneys In response to changes in plasma pH Body normally generates enough metabolic and fixed acids each day to add 100 mEq of H+ to ECF H+ are excreted in urine Kidneys assist lungs by eliminating any CO2 that Enters renal tubules during filtration Diffuses into tubular fluid en route to renal pelvis

27-5 Acid-Base Balance Hydrogen ions Secreted into tubular fluid along
Proximal convoluted tubule (PCT) Distal convoluted tubule (DCT) Collecting system

27-5 Acid-Base Balance Buffers in urine
Required to eliminate large numbers of H+ Glomerular filtration provides components of Carbonic acid–bicarbonate buffer system Phosphate buffer system Tubule cells of PCT Generate ammonia Ammonia buffer system

27-5 Acid-Base Balance Renal responses to acidosis Secretion of H+
Activity of buffers in tubular fluid Removal of CO2 Reabsorption of NaHCO3

27-5 Acid-Base Balance Renal responses to alkalosis
Rate of H+ secretion at kidneys declines Tubule cells do not reclaim bicarbonate ions in tubular fluid Collecting system transports HCO3– into tubular fluid while releasing H+ and Cl– into peritubular fluid

27-6 Disorders of Acid-Base Balance
Serious and prolonged disturbances of acid-base balance can result in Disorders affecting circulating buffers, respiratory performance, or renal function Cardiovascular conditions such as heart failure or hypotension Conditions affecting CNS Neural damage or disease can affect reflexes essential to pH regulation

Serious abnormalities in acid-base balance Acute phase Initial phase pH moves rapidly out of normal range Compensated phase When condition persists Physiological adjustments occur

Respiratory acid-base disorders Result from imbalance between CO2 generation in peripheral tissues CO2 excretion at lungs Cause abnormal CO2 levels in ECF Metabolic acid-base disorders Result from Generation of metabolic or fixed acids Conditions affecting HCO3– concentration in ECF

The response to acidosis caused by the addition of H+
Figure 27–14a Interactions among the Carbonic Acid–Bicarbonate Buffer System and Respiratory and Renal Compensation Mechanisms in the Regulation of Plasma pH. a The response to acidosis caused by the addition of H+ Addition of H+ Start CARBONIC ACID–BICARBONATE BUFFER SYSTEM BICARBONATE RESERVE CO2 CO2 + H2O H2CO3 (carbonic acid) H+ HCO3— (bicarbonate ion) + HCO3– + Na+ NaHCO3 (sodium bicarbonate) Lungs Generation of HCO3– Respiratory Response to Acidosis Other buffer systems absorb H+ Kidneys Renal Response to Acidosis Increased respiratory rate decreases PCO2, effectively converting carbonic acid molecules to water. Kidney tubules respond by (1) secreting H+, (2) removing CO2, and (3) reabsorbing HCO3– to help replenish the bicarbonate reserve. Secretion of H+

The response to acidosis caused by the addition of H+
Figure 27–14b Interactions among the Carbonic Acid–Bicarbonate Buffer System and Respiratory and Renal Compensation Mechanisms in the Regulation of Plasma pH. b The response to acidosis caused by the addition of H+ Removal of H+ Start CARBONIC ACID–BICARBONATE BUFFER SYSTEM BICARBONATE RESERVE Lungs CO2 + H2O H2CO3 (carbonic acid) H+ HCO3— (bicarbonate ion) + HCO3– + Na+ NaHCO3 (sodium bicarbonate) Respiratory Response to Alkalosis Other buffer systems release H+ Generation of H+ Kidneys Decreased respiratory rate increases PCO2, effectively converting CO2 molecules to carbonic acid. Renal Response to Alkalosis Kidney tubules respond by conserving H+ and secreting HCO3—. Secretion of HCO3—

Respiratory acidosis Develops when respiratory system cannot eliminate all CO2 generated by peripheral tissues Primary sign Low blood pH due to hypercapnia (high blood PCO2) Primary cause Hypoventilation (abnormally low respiratory rate)

Respiratory acidosis Acute respiratory acidosis Develops if decline in pH is severe Immediate, life-threatening condition Chronic respiratory acidosis Develops when normal respiratory function has been compromised Compensatory mechanisms have not failed completely

Respiratory alkalosis Primary sign High blood pH due to hypocapnia (low blood PCO2) Primary cause Hyperventilation (abnormally high respiratory rate)

Metabolic acidosis Three major causes High production of fixed or metabolic acids H+ overload buffer system Lactic acidosis After strenuous exercise or hypoxia Ketoacidosis In starvation and diabetes mellitus Impaired H+ excretion at kidneys Severe bicarbonate ion loss

Metabolic alkalosis Caused by elevated HCO3– concentrations Bicarbonate ions interact with H+ in solution Forming H2CO3 Decreased H+ concentration causes alkalosis

Figure 27–17 Responses to Metabolic Alkalosis.
HOMEOSTASIS NORMAL ACID-BASE BALANCE Homeostasis Homeostasis DISTURBED BY RESTORED BY STIMULUS RESTORED LOSS OF blood pH H+ or GAIN OF returning to Decreased H+ or increased HCO3– causes increased blood pH Responses to Metabolic Alkalosis HCO3– normal Kidneys generate H+ and secrete HCO3– Buffer systems other than the carbonic acid–bicarbonate system release H+ Increased H+ and decreased HCO3– Receptors Arterial and CSF chemoreceptors inhibited Decreased respiratory rate Increased PCO2 Metabolic alkalosis

Respiratory and metabolic acidosis Typically linked Low O2 results in generation of lactic acid Hypoventilation leads to low arterial PO2 Detection of acidosis and alkalosis Includes measuring pH, PCO2, PO2, and HCO3– levels in blood After diagnosis of acidosis or alkalosis, Condition is classified as respiratory or metabolic

27-7 Effects of Aging Fluid, electrolyte, and acid-base balance
Fetal pH control Buffers in fetal bloodstream provide short-term pH control Maternal kidneys eliminate H+ Newborn Body water content is high (75 percent of body weight) Basic aspects of electrolyte balance are the same as in adult

27-7 Effects of Aging Aging and fluid balance In a person under age 40
50–60 percent of body weight is water Body water content in people 40–60 years old 55 percent in males 47 percent in females After age 60 50 percent in males 45 percent in females

27-7 Effects of Aging Aging and fluid balance
Decreased body water content reduces dilution of wastes, toxins, and drugs Reduction in glomerular filtration rate and number of functional nephrons Reduces pH regulation by renal compensation Ability to concentrate urine declines More water is lost in urine Insensible perspiration increases as skin becomes thinner

27-7 Effects of Aging Aging and fluid balance
Maintaining fluid balance requires higher daily water intake Reduction in ADH and aldosterone sensitivity Reduces ability to conserve body water when losses exceed gains Muscle mass and skeletal mass decrease Causing net loss in body mineral content Loss can be prevented in part by exercise and increased dietary mineral supply

27-7 Effects of Aging Aging and acid-base balance
Reduction in vital capacity Reduces respiratory compensation Increases risk of respiratory acidosis Aggravated by arthritis and emphysema Disorders affecting major systems become more common with increasing age

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