Download Free Medical Fluid Electrolyte and Acid-Base Balance PowerPoint Presentation

Fluid Electrolyte and Acid-Base Balance PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "Fluid, Electrolyte, and Acid-Base Balance".

This medical PowerPoint presentation talks about fluid, electrolyte, and acid-base balance, essential functions that the body must maintain to stay healthy. These three systems work together to ensure that the bodys internal environment remains stable and functioning optimally.

Fluid balance refers to the regulation of the bodys water content. The body is made up of about 60% water, and maintaining the correct balance of fluids is crucial for many bodily functions, including regulating body temperature, transporting nutrients, and removing waste products. The body regulates fluid balance through the actions of the kidneys, which control the amount of water that is excreted or retained.

Electrolyte balance refers to the regulation of the bodys ions, including sodium, potassium, calcium, and magnesium. These ions are essential for many bodily functions, including nerve and muscle function, fluid balance, and pH regulation. The body maintains electrolyte balance through the actions of the kidneys, as well as through dietary intake.

Acid-base balance refers to the regulation of the pH of the bodys fluids, which must remain within a narrow range for optimal function. The body maintains acid-base balance through the actions of the lungs and kidneys, which regulate the concentration of carbon dioxide and bicarbonate ions in the blood.

Imbalances in any of these systems can have serious consequences for health. For example, dehydration can lead to kidney failure, electrolyte imbalances can cause muscle cramps and other symptoms, and acid-base imbalances can lead to acidosis or alkalosis, which can be life-threatening. Proper hydration, balanced electrolyte intake, and maintaining a healthy diet are all important for maintaining fluid, electrolyte, and acid-base balance in the body.

Tags : acid-Base Balance, Fluid balance refers, Electrolyte balance , Emergency Medicine, Emergency Medicine PowerPOint presentation

Published on : Apr 03, 2023 | Views : 1424 | Downloads : 13

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

24 Fluid, Electrolyte, and Acid-Base Balance
Slide 2-

Section 1: Fluid and Electrolyte Balance Learning Outcomes 24.1 Explain what is meant by fluid balance, and discuss its importance for homeostasis. 24.2 Explain what is meant by mineral balance, and discuss its importance for homeostasis. 24.3 Summarize the relationship between sodium and water in maintaining fluid and electrolyte balance. 24.4 CLINICAL MODULE Explain factors that control potassium balance, and discuss hypokalemia and hyperkalemia.
Slide 3-

Section 1: Fluid and Electrolyte Balance Fluids constitute ~50%–60% of total body composition Minerals (inorganic substances) are dissolved within and form ions called electrolytes Fluid compartments Intracellular fluid (ICF) Water content varies most here due to variation in: Tissue types (muscle vs. fat) Distinct from ECF due to plasma membrane transport Extracellular fluid (ECF) Interstitial fluid volume varies Volume of blood (women < men)
Slide 4-

Figure 24 Section 1 1 Total body composition of adult males Total body composition of adult males and females Total body composition of adult females Intracellularfluid 33% Interstitialfluid 21.5% Plasma 4.5% Solids 40%(organic and inorganic materials) Other body fluids (≤1%) Adult males ICF ECF Other body fluids (≤1%) Interstitialfluid 18% Intracellularfluid 27% Plasma 4.5% Solids 50%(organic and inorganic materials) ICF ECF Adult females WATER 60% WATER 50% SOLIDS 40% SOLIDS 50%
Slide 5-

Figure 24 Section 1 2 SOLID COMPONENTS The solid components of a 70-kg (154-pound)individual with a minimum of body fat (31.5 kg; 69.3 lbs) Kg Proteins Lipids Minerals Carbohydrates Miscellaneous
Slide 6-

Module 24.1: Fluid balance Fluid balance Water content stable over time Gains Primarily absorption along digestive tract As nutrients and ions are absorbed, osmotic gradient created causing passive absorption of water Losses Mainly through urination (over 50%) but other routes as well Digestive secretions are reabsorbed similarly to ingested fluids
Slide 7-

Figure 24.1 1
Slide 8-

Figure 24.1 2 Dietary Input Digestive Secretions Water Reabsorption Food and drink 2200 mL The digestive tract sites of water gainthrough ingestion or secretion, or waterreabsorption, and of water loss Small intestinereabsorbs 8000 mL Colon reabsorbs 1250 mL 150 mL lostin feces 1400mL 1200 mL 9200 mL 5200 mL Colonic mucous secretions200 mL Intestinal secretions 2000 mL Liver (bile) 1000 mLPancreas (pancreaticjuice) 1000 mL Gastric secretions 1500 mL Saliva 1500 mL
Slide 9-

Module 24.1: Fluid balance ICF and ECF compartments balance Very different composition Are at osmotic equilibrium Loss of water from ECF is replaced by water in ICF = Fluid shift Occurs in minutes to hours and restores osmotic equilibrium Dehydration Results in long-term transfer that cannot replace ECF water loss Homeostatic mechanisms to increase ECF fluid volume will be employed
Slide 10-

Figure 24.1 3 The major factors that affect ECF volume ICF ECF Water absorbed acrossdigestive epithelium(2000 mL) Metabolicwater(300 mL) Water vapor lost in respiration andevaporation frommoist surfaces(1150 mL) Water lost in feces (150 mL) Water secretedby sweat glands(variable) Water lost in urine(1000 mL) Plasma membranes
Slide 11-

Figure 24.1 4 Changes to the ICF and ECF when water losses outpace water gains Intracellularfluid (ICF) Extracellularfluid (ECF) The ECF and ICF are inbalance, with the twosolutions isotonic. ECF water loss Water loss from ECFreduces volume andmakes this solutionhypertonic with respectto the ICF. IncreasedECF volume Decreased ICF volume An osmotic water shiftfrom the ICF into theECF restores osmoticequilibrium butreduces the ICF volume.
Slide 12-

Module 24.1 Review a. Identify routes of fluid loss from the body. b. Describe a fluid shift. c. Explain dehydration and its effect on the osmotic concentration of plasma.
Slide 13-

Module 24.2: Mineral balance Mineral balance Equilibrium between ion absorption and excretion Major ion absorption through intestine and colon Major ion excretion by kidneys Sweat glands excrete ions and water variably Ion reserves mainly in skeleton
Slide 14-

Figure 24.2 1 Mineral balance, the balance between ion absorption (in the digestive tract) and ion excretion (primarily at the kidneys) Ion Absorption Ion Excretion ICF ECF Ion absorption occurs across theepithelial lining of the small intestineand colon. Ion reserves (primarilyin the skeleton) Ion pool in body fluids Sweat glandsecretions(secondarysite of ion loss) Kidneys(primary siteof ion loss)
Slide 15-

Figure 24.2 2
Slide 16-

Figure 24.2 3
Slide 17-

Figure 24.2 3
Slide 18-

Module 24.2 Review a. Define mineral balance. b. Identify the significance of two important body minerals: sodium and calcium. c. Identify the ions absorbed by active transport.
Slide 19-

Module 24.3: Water and sodium balance Sodium balance (when sodium gains equal losses) Relatively small changes in Na+ are accommodated by changes in ECF volume Homeostatic responses involve two parts ADH control of water loss/retention by kidneys and thirst Fluid exchange between ECF and ICF
Slide 20-

Figure 24.3 1 The mechanisms that regulate sodium balancewhen sodium concentration in the ECF changes Rising plasmasodium levels The secretion of ADHrestricts water loss andstimulates thirst, promotingadditional waterconsumption. Osmoreceptorsin hypothalamusstimulated HOMEOSTASISDISTURBED Increased Nalevels in ECF If you consume largeamounts of salt withoutadequate fluid, as whenyou eat salty potatochips without taking a drink, the plasma Naconcentration rises temporarily. ADH Secretion Increases Recall of Fluids Because the ECFosmolarity increases,water shifts out of the ICF, increasing ECFvolume and lowering ECF Na concentrations. HOMEOSTASISRESTORED Decreased Nalevels in ECF HOMEOSTASIS Normal Naconcentrationin ECF Start
Slide 21-

Figure 24.3 1 The mechanisms that regulate sodium balancewhen sodium concentration in the ECF changes Falling plasmasodium levels HOMEOSTASIS Normal Naconcentrationin ECF Start HOMEOSTASISRESTORED Increased Nalevels in ECF HOMEOSTASISDISTURBED Decreased Nalevels in ECF ADH SecretionDecreases Osmoreceptorsin hypothalamusinhibited Water loss reducesECF volume,concentrates ions As soon as the osmoticconcentration of the ECFdrops by 2 percent ormore, ADH secretiondecreases, so thirst issuppressed and waterlosses at the kidneysincrease.
Slide 22-

Module 24.3: Water and sodium balance Sodium balance (continued) Exchange changes in Na+ are accommodated by changes in blood pressure and volume Hyponatremia (natrium, sodium) Low ECF Na+ concentration (<136 mEq/L) Can occur from overhydration or inadequate salt intake Hypernatremia High ECF Na+ concentration (>145 mEq/L) Commonly from dehydration
Slide 23-

Module 24.3: Water and sodium balance Sodium balance (continued) Exchange changes in Na+ are accommodated by changes in blood pressure and volume (continued) Increased blood volume and pressure Natriuretic peptides released Increased Na+ and water loss in urine Reduced thirst Inhibition of ADH, aldosterone, epinephrine, and norepinephrine release Decreased blood volume and pressure Endocrine response Increased ADH, aldosterone, RAAS mechanism Opposite bodily responses to above
Slide 24-

Figure 24.3 2 Rising bloodpressure andvolume HOMEOSTASIS Normal ECFvolume HOMEOSTASISRESTORED Falling ECF volume HOMEOSTASISDISTURBED Rising ECF volume by fluidgain or fluid and Na gain Combined Effects Responses to Natriuretic Peptides Increased bloodvolume andatrial distension Natriuretic peptidesreleased by cardiacmuscle cells The mechanisms that regulate water balancewhen ECF volume changes Increased Na loss in urine Increased water loss in urine Reduced thirst Inhibition of ADH, aldosterone,epinephrine, and norepinephrinerelease Reduced bloodvolume Reduced bloodpressure Start
Slide 25-

Figure 24.3 2 Falling bloodpressure andvolume HOMEOSTASIS Normal ECFvolume Endocrine Responses Increased renin secretionand angiotensin IIactivation Combined Effects Increased aldosteronerelease Increased ADH release Increased urinary Na retention Decreased urinary water loss Increased thirst Increased water intake Decreased bloodvolume andblood pressure HOMEOSTASISDISTURBED Falling ECF volume by fluidloss or fluid and Na loss HOMEOSTASISRESTORED Rising ECF volume Start The mechanisms that regulate water balancewhen ECF volume changes
Slide 26-

Module 24.3 Review a. What effect does inhibition of osmoreceptors have on ADH secretion and thirst? b. What effect does aldosterone have on sodium ion concentration in the ECF? c. Briefly summarize the relationship between sodium ion concentration and the ECF.
Slide 27-

CLINICAL MODULE 24.4: Potassium imbalance Potassium balance (K+ gain = loss) Major gain is through digestive tract absorption ~100 mEq (1.9–5.8 g)/day Major loss is excretion by kidneys Primary ECF potassium regulation by kidneys since intake fairly constant Controlled by aldosterone regulating Na+/K+ exchange pumps in DCT and collecting duct of nephron Low ECF pH can cause H+ to be substituted for K+ Potassium is highest in ICF due to Na+/K+ exchange pump ~135 mEq/L in ICF vs. ~5 mEq/L in ECF
Slide 28-

Figure 24.4 1 The major factors involved in potassium balance Factors Controlling Potassium Balance Approximately 100mEq (1.9–5.8 g) ofpotassium ions are absorbed by thedigestive tract eachday. Roughly 98 percent of thepotassiumcontent of thehuman body is inthe ICF, ratherthan the ECF. The K concentration in theECF is relatively low. The rateof K entry from the ICFthrough leak channels isbalanced by the rate of Krecovery by the Na/Kexchange pump. When potassiumbalance exists,the rate of urinaryK excretionmatches the rateof digestive tractabsorption. The potassium ionconcentration in theECF is approximately5 mEq/L. KEY  Absorption  Secretion  Diffusion through leak channels The potassium ionconcentration of theICF is approximately135 mEq/L. Renal K lossesare approximately100 mEq per day
Slide 29-

Figure 24.4 2 The role of aldosterone-sensitive exchange pumpsin the kidneys in determining the potassiumconcentration in the ECF The primary mechanism ofpotassium secretion involvesan exchange pump thatejects potassium ions whilereabsorbing sodium ions. Tubularfluid  Sodium-potassium exchange pump  Aldosterone- sensitive exchange pump The sodium ions are then pumped outof the cell in exchange for potassiumions in the ECF. This is the same pumpthat ejects sodium ions entering thecytosol through leak channels. KEY ECF
Slide 30-

Figure 24.4 3 Events in the kidneys that affect potassium balance Under normal conditions, thealdosterone-sensitive pumpsexchange K in the ECF forNa in the tubular fluid. Thenet result is a rise in plasmasodium levels and increasedK loss in the urine. When the pH falls in the ECFand the concentration of H isrelatively high, the exchangepumps bind H instead of K.This helps to stabilize the pHof the ECF, but at the cost ofrising K levels in the ECF. Distalconvolutedtubule Collectingduct
Slide 31-

Disturbances of potassium balance Hypokalemia (kalium, potassium) Below 2 mEq/L in plasma Can be caused by: Diuretics Aldosteronism (excessive aldosterone secretion) Symptoms Muscular weakness, followed by paralysis Potentially lethal when affecting heart CLINICAL MODULE 24.4: Potassium imbalance
Slide 32-

Disturbances of potassium balance (continued) Hyperkalemia Above 8 mEq/L in plasma Can be caused by: Chronically low pH Kidney failure Drugs promoting diuresis by blocking Na+/K+ pumps Symptoms Muscular spasm including heart arrhythmias CLINICAL MODULE 24.4: Potassium imbalance
Slide 33-

CLINICAL MODULE 24.4 Review a. Define hypokalemia and hyperkalemia. b. What organs are primarily responsible for regulating the potassium ion concentration of the ECF? c. Identify factors that cause potassium excretion.
Slide 34-

Section 2: Acid-Base Balance Learning Outcomes 24.5 Explain the role of buffer systems in maintaining acid-base balance and pH. 24.6 Explain the role of buffer systems in regulating the pH of the intracellular fluid and the extracellular fluid. 24.7 Describe the compensatory mechanisms involved in the maintenance of acid-base balance. 24.8 CLINICAL MODULE Describe respiratory acidosis and respiratory alkalosis.
Slide 35-

Section 2: Acid-Base Balance Acid-base balance (H+ production = loss) Normal plasma pH: 7.35–7.45 H+ gains: many metabolic activities produce acids CO2 (to carbonic acid) from aerobic respiration Lactic acid from glycolysis H+ losses and storage Respiratory system eliminates CO2 H+ excretion from kidneys Buffers temporarily store H+
Slide 36-

Figure 24 Section 2 1 The major factors involved in the maintenanceof acid-base balance Active tissuescontinuously generatecarbon dioxide, which insolution forms carbonicacid. Additional acids,such as lactic acid, areproduced in the course ofnormal metabolicoperations. Tissue cells Buffer Systems Normalplasma pH(7.35–7.45) Buffer systems cantemporarily store Hand thereby provideshort-term pHstability. The respiratory systemplays a key role byeliminatingcarbon dioxide. The kidneys play a majorrole by secretinghydrogen ions into the urine and generatingbuffers that enter thebloodstream. The rate ofexcretion rises and fallsas needed to maintainnormal plasma pH. As a result, the normal pH ofurine varies widely butaverages 6.0—slightlyacidic.
Slide 37-

Section 2: Acid-Base Balance Classes of acids Fixed acids Do not leave solution Remain in body fluids until kidney excretion Examples: sulfuric and phosphoric acid Generated during catabolism of amino acids, phospholipids, and nucleic acids Organic acids Part of cellular metabolism Examples: lactic acid and ketones Most metabolized rapidly so no accumulation
Slide 38-

Section 2: Acid-Base Balance Classes of acids (continued) Volatile acids Can leave body by external respiration Example: carbonic acid (H2CO3)
Slide 39-

Module 24.5: Buffer systems pH imbalance ECH pH normally between 7.35 and 7.45 Acidemia (plasma pH <7.35): acidosis (physiological state) More common due to acid-producing metabolic activities Effects CNS function deteriorates, may cause coma Cardiac contractions grow weak and irregular Peripheral vasodilation causes BP drop Alkalemia (plasma pH >7.45): alkalosis (physiological state) Can be dangerous but relatively rare
Slide 40-

Figure 24.5 1
Slide 41-

Figure 24.5 2 The narrow range of normal pH of the ECF, and the conditions that result from pH shifts outside the normal range The pH of the ECF(extracellular fluid)normally ranges from7.35 to 7.45. pH When the pH of plasma falls below7.5, acidemia exists. Thephysiological state that results iscalled acidosis. When the pH of plasma risesabove 7.45, alkalemia exists.The physiological state thatresults is called alkalosis. Severe acidosis (pH below 7.0) can be deadlybecause (1) central nervous system functiondeteriorates, and the individual may becomecomatose; (2) cardiac contractions grow weak andirregular, and signs and symptoms of heart failuremay develop; and (3) peripheral vasodilationproduces a dramatic drop in blood pressure,potentially producing circulatory collapse. Severe alkalosis is alsodangerous, but serious casesare relatively rare. Extremelyacidic Extremelybasic
Slide 42-

Module 24.5: Buffer systems CO2 partial pressure effects on pH Most important factor affecting body pH H2O + CO2  H2CO3  H+ + HCO3– Reversible reaction that can buffer body pH Adjustments in respiratory rate can affect body pH
Slide 43-

Figure 24.5 3 When carbon dioxide levels rise, more carbonic acidforms, additional hydrogen ions and bicarbonate ionsare released, and the pH goes down. When the PCO2 falls, the reaction runs in reverse, andcarbonic acid dissociates into carbon dioxide andwater. This removes H ions from solution andincreases the pH. If PCO2 rises If PCO2 falls PCO240–45mm Hg pH7.35–7.45 The inverse relationship between the PCO2 and pH HOMEOSTASIS H2O  CO2 H2CO3 H  HCO3 H  HCO3 H2CO3 H2O  CO2 PCO2 PCO2 pH pH
Slide 44-

Module 24.5: Buffer systems Buffer Substance that opposes changes to pH by removing or adding H+ Generally consists of: Weak acid (HY) Anion released by its dissociation (Y–) HY  H+ + Y– and H+ + Y–  HY
Slide 45-

Figure 24.5 4 The reactions that occur when pH buffer systems function A buffer system in body fluids generallyconsists of a combination of a weak acid (HY) and the anion (Y) released by its dissociation.The anion functions as a weak base. In solution,molecules of the weak acid exist in equilibriumwith its dissociation products. Adding H to thesolution upsets the equilibrium and resultsin the formation ofadditional molecules ofthe weak acid. Removing H from thesolution also upsets theequilibrium and results in the dissociation ofadditional molecules ofHY. This releases H.
Slide 46-

Module 24.5 Review a. Define acidemia and alkalemia. b. What is the most important factor affecting the pH of the ECF? c. Summarize the relationship between CO2 levels and pH.
Slide 47-

Module 24.6: Major body buffer systems Three major body buffer systems All can only temporarily affect pH (H+ not eliminated) Phosphate buffer system Buffers pH of ICF and urine Carbonic acid–bicarbonate buffer system Most important in ECF Fully reversible Bicarbonate reserves (from NaHCO3 in ECF) contribute
Slide 48-

Module 24.6: Major body buffer systems Three major body buffer systems (continued) Protein buffer systems (in ICF and ECF) Usually operate under acid conditions (bind H+) Binding to carboxyl group (COOH–) and amino group (—NH2) Examples: Hemoglobin buffer system CO2 + H2O  H2CO3  HCO3– + Hb-H+ Only intracellular system with immediate effects Amino acid buffers (all proteins) Plasma proteins
Slide 49-

Figure 24.6 1 The body’s three major buffer systems Buffer Systems Intracellular fluid (ICF) Extracellular fluid (ECF) occur in Phosphate BufferSystem Protein Buffer Systems Carbonic Acid–Bicarbonate Buffer System Has an importantrole in buffering thepH of the ICF andof urine Contribute to the regulation of pH in the ECF and ICF;interact extensively with the other two buffer systems Is most important in theECF Hemoglobinbuffer system(RBCs only) Amino acidbuffers(All proteins) Plasmaproteinbuffers
Slide 50-

Figure 24.6 4 The reactions of the carbonic acid–bicarbonate buffer system CARBONIC ACID–BICARBONATEBUFFER SYSTEM BICARBONATE RESERVE Start CO2 CO2  H2O H2CO3(carbonic acid) H  HCO3 (bicarbonate ion) NaHCO3(sodium bicarbonate) HCO3  Na Body fluids contain a large reserve ofHCO3, primarily in the form of dissolvedmolecules of the weak base sodiumbicarbonate (NaHCO3). This readilyavailable supply of HCO3 is known asthe bicarbonate reserve. Addition of Hfrom metabolicactivity The primary function of the carbonicacid–bicarbonate buffer system is toprotect against the effects of the organicand fixed acids generated throughmetabolic activity. In effect, it takes the H released by these acids and generatescarbonic acid that dissociates into waterand carbon dioxide, which can easily be eliminated at the lungs. Lungs
Slide 51-

Figure 24.6 2 The events involved in the functioning of the hemoglobin buffer system Tissuecells Plasma Plasma Lungs Red blood cells Red blood cells Releasedwithexhalation CO2 H2O H2CO3 HCO3  Hb H H  HCO3 Hb H2CO3 H2O CO2
Slide 52-

Figure 24.6 3 The mechanism by free amino acids function inprotein buffer systems Start Normal pH(7.35–7.45) Increasing acidity (decreasing pH) At the normal pH ofbody fluids (7.35–7.45), the carboxylgroups of most amino acids have releasedtheir hydrogen ions. If pH drops, the carboxylate ion (COO)and the amino group (—NH2) of a freeamino acid can act as weak bases andaccept additional hydrogen ions, forming acarboxyl group (—COOH) and an aminoion (—NH3), respectively. Many of theR-groups can also accept hydrogen ions,forming RH.
Slide 53-

Module 24.6: Major body buffer systems Disorders Metabolic acid-base disorders Production or loss of excessive amounts of fixed or organic acids Carbonic acid–bicarbonate system works to counter Respiratory acid-base disorders Imbalance of CO2 generation and elimination Must be corrected by depth and rate of respiration changes
Slide 54-

Module 24.6 Review a. Identify the body’s three major buffer systems. b. Describe the carbonic acid–bicarbonate buffer system. c. Describe the roles of the phosphate buffer system.
Slide 55-

Module 24.7: Metabolic acid-base disorders Metabolic acid-base disorders Metabolic acidosis Develops when large numbers of H+ are released by organic or fixed acids Accommodated by respiratory and renal responses Respiratory response Increased respiratory rate lowers PCO2 H+ + HCO3–  H2CO3  H2O + CO2 Renal response Occurs in PCT, DCT, and collecting system H2O + CO2  H2CO3  H+ + HCO3–  H+ secreted into urine  HCO3– reabsorbed into ECF
Slide 56-

Figure 24.7 1 The responses to metabolic acidosis Additionof H Start CO2 CO2  H2O H2CO3(carbonic acid) H  HCO3 Lungs (bicarbonate ion) HCO3  Na NaHCO3(sodium bicarbonate) Generationof HCO3 CARBONIC ACID–BICARBONATE BUFFER SYSTEM BICARBONATE RESERVE Respiratory Responseto Acidosis Renal Response to Acidosis Otherbuffersystemsabsorb H KIDNEYS Secretionof H Increased respiratoryrate lowers PCO2,effectively convertingcarbonic acid moleculesto water. Kidney tubules respond by (1) secreting Hions, (2) removing CO2, and (3) reabsorbingHCO3 to help replenish the bicarbonatereserve.
Slide 57-

Figure 24.7 2 The activity of renaltubule cells in CO2removal and HCO3 production Tubularfluid Renal tubule cells ECF H H H H Na Na CO2 CO2 HCO3 HCO3 H2CO3 HCO3 CO2  H2O Cl Cl Carbonicanhydrase CO2 generated by the tubulecell is added to the CO2diffusing into the cell fromthe urine and from the ECF. Steps in CO2 removal andHCO3 production Carbonic anhydraseconverts CO2 and water tocarbonic acid, which then dissociates. The chloride ions exchangedfor bicarbonate ions areexcreted in the tubular fluid. Bicarbonate ions andsodium ions are transportedinto the ECF, adding to thebicarbonate reserve.
Slide 58-

Module 24.7: Metabolic acid-base disorders Metabolic alkalosis Develops when large numbers of H+ are removed from body fluids Rate of kidney H+ secretion declines Tubular cells do not reclaim bicarbonate Collecting system transports bicarbonate into urine and retains acid (HCl) in ECF
Slide 59-

Module 24.7: Metabolic acid-base disorders Metabolic alkalosis (continued) Accommodated by respiratory and renal responses Respiratory response Decreased respiratory rate raises PCO2 H2O + CO2  H2CO3  H+ + HCO3– Renal response Occurs in PCT, DCT, and collecting system H2O + CO2  H2CO3  H+ + HCO3– HCO3– secreted into urine (in exchange for Cl–) H+ actively reabsorbed into ECF
Slide 60-

Figure 24.7 3 The responses to metabolic alkalosis Start Lungs Removalof H CO2  H2O H  HCO3 H2CO3(carbonic acid) HCO3  Na NaHCO3(sodium bicarbonate) (bicarbonate ion) CARBONIC ACID–BICARBONATE BUFFER SYSTEM BICARBONATE RESERVE Generationof H KIDNEYS Secretionof HCO3 Otherbuffersystemsrelease H Respiratory Responseto Alkalosis Renal Response to Alkalosis Decreased respiratoryrate elevates PCO2,effectively convertingCO2 molecules tocarbonic acid. Kidney tubules respond byconserving H ions and secreting HCO3.
Slide 61-

Figure 24.7 4 The events in thesecretion of bicarbonateions into the tubularfluid along the PCT, DCT,and collecting system Tubularfluid Renal tubule cells ECF H2CO3 CO2  H2O Carbonicanhydrase H CO2 HCO3 H HCO3 CO2 Cl Cl CO2 generated by the tubulecell is added to the CO2diffusing into the cell from thetubular fluid and from the ECF. Carbonic anyhydrase convertsCO2 and water to carbonic acid, which then dissociates. The hydrogen ions are activelytransported into the ECF,accompanied by the diffusionof chloride ions. HCO3 is pumped into thetubular fluid in exchange forchloride ions that will diffuseinto the ECF.
Slide 62-

Module 24.7 Review a. Describe metabolic acidosis. b. Describe metabolic alkalosis. c. lf the kidneys are conserving HCO3– and eliminating H+ in acidic urine, which is occurring: metabolic alkalosis or metabolic acidosis?
Slide 63-

CLINICAL MODULE 24.8: Respiratory acid-base disorders Respiratory acid-base disorders Respiratory acidosis CO2 generation outpaces rate of CO2 elimination at lungs Shifts bicarbonate buffer system toward generating more carbonic acid H2O + CO2  H2CO3  H+ + HCO3– HCO3– goes into bicarbonate reserve H+ must be neutralized by any of the buffer systems Respiratory (increased respiratory rate) Renal (H+ secreted and HCO3– reabsorbed) Proteins (bind free H+)
Slide 64-

Figure 24.8 1 The events in respiratory acidosis CARBONIC ACID–BICARBONATEBUFFER SYSTEM BICARBONATE RESERVE Lungs CO2 CO2  H2O H2CO2(carbonic acid) H  HCO3 (bicarbonate ion) HCO3  Na NaHCO3(sodium bicarbonate) When respiratory activity does not keeppace with the rate of CO2 generation,alveolar and plasma PCO2 increases.This upsets the equilibrium and drivesthe reaction to the right, generatingadditional H2CO3, which releases Hand lowers plasma pH. As bicarbonate ions and hydrogen ionsare released through the dissociation ofcarbonic acid, the excess bicarbonateions become part of the bicarbonatereserve. To limit the pH effects ofrespiratory acidosis, the excess H must either be tied up byother buffer systems or excreted at the kidneys. The underlyingproblem, however, cannot beeliminated without an increase inthe respiratory rate.
Slide 65-

Figure 24.8 2 The integrated homeostatic responsesto respiratory acidosis IncreasedPCO2 Elevated PCO2 resultsin a fall in plasma pH Respiratory Acidosis Responses to Acidosis Combined Effects Respiratory compensation Renal compensation Decreased PCO2 Decreased H andincreased HCO3 Stimulation of arterial and CSFchemoreceptors results inincreased respiratory rate. H ions are secreted andHCO3 ions are generated. Buffer systems other than thecarbonic acid–bicarbonatesystem accept H ions. HOMEOSTASISDISTURBED HOMEOSTASISRESTORED Hypoventilationcausing increased PCO2 Plasma pHreturns to normal Start Normal acid-base balance HOMEOSTASIS
Slide 66-

CLINICAL MODULE 24.8: Respiratory acid-base disorders Respiratory alkalosis CO2 elimination at lungs outpaces CO2 generation rate Shifts bicarbonate buffer system toward generating more carbonic acid H+ + HCO3–  H2CO3  H2O + CO2 H+ removed as CO2 exhaled and water formed Buffer system responses Respiratory (decreased respiratory rate) Renal (HCO3– secreted and H+ reabsorbed) Proteins (release free H+)
Slide 67-

Figure 24.8 3 The events in respiratory alkalosis If respiratory activity exceeds the rate of CO2 generation, alveolar and plasma PCO2 decline,and this disturbs the equilibrium and drivesthe reactions to the left, removing H and elevating plasma pH. CO2 CO2  H2O H2CO2(carbonic acid) H  HCO3 (bicarbonate ion) HCO3  Na NaHCO3(sodium bicarbonate) Lungs CARBONIC ACID–BICARBONATEBUFFER SYSTEM BICARBONATE RESERVE As bicarbonate ions and hydrogenions are removed in the formation ofcarbonic acid, the bicarbonate ions—but not the hydrogen ions—arereplaced by the bicarbonate reserve.
Slide 68-

Figure 24.8 4 The integrated homeostatic responses torespiratory alkalosis Start Normal acid-base balance HOMEOSTASIS DecreasedPCO2 Lower PCO2 resultsin a rise in plasma pH Respiratory Alkalosis HOMEOSTASISDISTURBED Hyperventilationcausing decreased PCO2 Plasma pHreturns to normal HOMEOSTASISRESTORED Increased PCO2 Combined Effects Increased H anddecreased HCO3 Responses to Alkalosis Respiratory compensation Renal compensation Inhibition of arterial and CSFchemoreceptors results in adecreased respiratory rate. H ions are generated and HCO3 ions are secreted. Buffer systems other than thecarbonic acid–bicarbonate systemrelease H ions.
Slide 69-

CLINICAL MODULE 24.8 Review a. Define respiratory acidosis and respiratory alkalosis. b. What would happen to the plasma PCO2 of a patient who has an airway obstruction? c. How would a decrease in the pH of body fluids affect the respiratory rate?