1. © 2012 Pearson Education, Inc. Figure 27-1a The Composition of the Human Body SOLID COMPONENTS (31.5 kg; 69.3 lbs) ProteinsLipidsMineralsCarbohydratesMiscellaneous Kg The body composition (by weight, averaged for both sexes) and major body fluid compartments of a 70-kg individual. p. 999

2. © 2012 Pearson Education, Inc. Figure 27-1a The Composition of the Human Body Liters Intracellular fluidExtracellular fluid Interstitial fluid Plasma Other WATER (38.5 kg; 84.7 lbs) The body composition (by weight, averaged for both sexes) and major body fluid compartments of a 70-kg individual. p. 999

3. © 2012 Pearson Education, Inc. Figure 27-1b The Composition of the Human Body A comparison of the body compositions of adult males and females, ages 18–40 years. Intracellular fluid 33% Interstitial fluid 21.5% WATER 60% SOLIDS 40% Other body fluids (  1%) Plasma 4.5% Solids 40% (organic and inorganic materials) Adult males ECF ICF p. 999

4. © 2012 Pearson Education, Inc. Figure 27-1b The Composition of the Human Body A comparison of the body compositions of adult males and females, ages 18–40 years. ECF ICF Adult females SOLIDS 50% Solids 50% (organic and inorganic materials) Intracellular fluid 27% Interstitial fluid 18% Other body fluids (  1%) Plasma 4.5% WATER 50% p. 999

5. © 2012 Pearson Education, Inc. Figure 27-2 Cations and Anions in Body Fluids CATIONS ECF ICF KEY Cations Plasma Interstitial fluid Intracellular fluid Milliequivalents per liter (mEq/L) Na  Ca 2  Mg 2  KK KK KK Na  KK Ca 2  Mg 2  p. 1001

6. © 2012 Pearson Education, Inc. Figure 27-2 Cations and Anions in Body Fluids KEY Anions ANIONS ECFICF Plasma Interstitial fluid Intracellular fluid Proteins Org. acid HPO 4 2  Cl  HCO 3  Organic acid Proteins HCO 3  Cl  HPO 4 2  SO 4 2  HCO 3  Cl  HPO 4 2  SO 4 2  HCO 3  Cl  HPO 4 2  p. 1001

7. Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings © 2012 Pearson Education, Inc. p. 1001

8. Normal Sodium Concentrations In ECF ~140 mEq/L In ICF ~ 10 mEq/L or less Normal Potassium Concentrations In ICF ~ 160 mEq/L In ECF ~ 3.5–5.5 mEq/L Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings © 2012 Pearson Education, Inc.

9. p. 1007 Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings © 2012 Pearson Education, Inc.

10. Figure 27-5 The Homeostatic Regulation of Normal Sodium Ion Concentrations in Body Fluids The secretion of ADH restricts water loss and stimulates thirst, promoting additional water consumption. Osmoreceptors in hypothalamus stimulated HOMEOSTASIS DISTURBED Increased Na  levels in ECF Because the ECF osmolarity increases, water shifts out of the ICF, increasing ECF volume and lowering Na  concentrations. HOMEOSTASIS RESTORED Decreased Na  levels in ECF Recall of Fluids ADH Secretion Increases HOMEOSTASIS Normal Na  concentration in ECF Start p. 1007

11. © 2012 Pearson Education, Inc. Figure 27-5 The Homeostatic Regulation of Normal Sodium Ion Concentrations in Body Fluids HOMEOSTASIS DISTURBED Decreased Na  levels in ECF Normal Na  concentration in ECF HOMEOSTASIS RESTORED Increased Na  levels in ECF Water loss reduces ECF volume, concentrates ions Osmoreceptors in hypothalamus inhibited As soon as the osmotic concentration of the ECF drops by 2 percent or more, ADH secretion decreases, so thirst is suppressed and water losses at the kidneys increase. Start ADH Secretion Decreases p. 1007

12. p. 1008 Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings © 2012 Pearson Education, Inc.

13. Figure 27-6 The Integration of Fluid Volume Regulation and Sodium Ion Concentrations in Body Fluids Natriuretic peptides released by cardiac muscle cells Rising blood pressure and volume Increased blood volume and atrial distension HOMEOSTASIS DISTURBED Rising ECF volume by fluid gain or fluid and Na  gain HOMEOSTASIS RESTORED Falling ECF volume Start HOMEOSTASIS Normal ECF volume Reduced blood volume Combined Effects Reduced blood pressure Increased Na  loss in urine Responses to Natriuretic Peptides Increased water loss in urine Reduced thirst Inhibition of ADH, aldosterone, epinephrine, and norepinephrine release p. 1008

14. © 2012 Pearson Education, Inc. Figure 27-6 The Integration of Fluid Volume Regulation and Sodium Ion Concentrations in Body Fluids HOMEOSTASIS DISTURBED Falling ECF volume by fluid loss or fluid and Na  loss Decreased blood volume and blood pressure Increased renin secretion and angiotensin II activation Increased aldosterone release Increased ADH release Increased urinary Na  retention Endocrine Responses Combined Effects Decreased urinary water loss Increased thirst Increased water intake Rising ECF volume HOMEOSTASIS RESTORED Start HOMEOSTASIS Normal ECF volume Falling blood pressure and volume p. 1008

15. © 2012 Pearson Education, Inc. Figure 27-9 The Basic Relationship between P CO 2 and Plasma pH P CO 2 40–45 mm Hg HOMEOSTASIS If P CO 2 rises When carbon dioxide levels rise, more carbonic acid forms, additional hydrogen ions and bicarbonate ions are released, and the pH goes down. P CO 2 pH H2OH2O  CO 2 H 2 CO 3 HCO 3  HH  p. 1013

16. © 2012 Pearson Education, Inc. Figure 27-9 The Basic Relationship between P CO 2 and Plasma pH pH P CO 2 When the P CO 2 falls, the reaction runs in reverse, and carbonic acid dissociates into carbon dioxide and water. This removes H  ions from solution and increases the pH. pH 7.35–7.45 HOMEOSTASIS If P CO 2 falls HH  HCO 3  H 2 CO 3 H2OH2OCO 2  p. 1013

17. © 2012 Pearson Education, Inc. Figure 27-10 Buffer Systems in Body Fluids Buffer Systems Intracellular fluid (ICF) Phosphate Buffer System Protein Buffer Systems The phosphate buffer system has an important role in buffering the pH of the ICF and of urine. 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. Hemoglobin buffer system (RBCs only) Amino acid buffers (All proteins) Plasma protein buffers The carbonic acid– bicarbonate buffer system is most important in the ECF. Carbonic Acid– Bicarbonate Buffer System Extracellular fluid (ECF) occur in p. 1014

18. © 2012 Pearson Education, Inc. Figure 27-11 The Role of Amino Acids in Protein Buffer Systems Neutral pH If pH fallsIf pH rises Amino acid In alkaline medium, amino acid acts as an acid and releases H  In acidic medium, amino acid acts as a base and absorbs H  p. 1014

19. © 2012 Pearson Education, Inc. Figure 23-24 A Summary of the Primary Gas Transport Mechanisms Systemic capillary Cells in peripheral tissues Chloride shift CO 2 pickup

20. © 2012 Pearson Education, Inc. Figure 23-24 A Summary of the Primary Gas Transport Mechanisms Alveolar air space Pulmonary capillary CO 2 delivery

21. © 2012 Pearson Education, Inc. Figure 27-12a The Carbonic Acid–Bicarbonate Buffer System CARBONIC ACID–BICARBONATE BUFFER SYSTEM H 2 CO 3 (carbonic acid) CO 2  H 2 O CO 2 Lungs Basic components of the carbonic acid–bicarbonate buffer system, and their relationships to carbon dioxide and the bicarbonate reserve HCO 3  (bicarbonate ion)  HH BICARBONATE RESERVE Na  HCO 3  NaHCO 3 (sodium bicarbonate) p. 1015

22. © 2012 Pearson Education, Inc. Figure 27-12b The Carbonic Acid–Bicarbonate Buffer System Fixed acids or organic acids: add H  The response of the carbonic acid–bicarbonate buffer system to hydrogen ions generated by fixed or organic acids in body fluids CO 2 Lungs CO 2  H 2 O Increased H 2 CO 3 HCO 3 – HH  Na  HCO 3  NaHCO 3 p. 1015

23. © 2012 Pearson Education, Inc. Figure 27-13a Kidney Tubules and pH Regulation The three major buffering systems in tubular fluid, which are essential to the secretion of hydrogen ions Cells of PCT, DCT, and collecting system Peritubular fluid Peritubular capillary Carbonic acid–bicarbonate buffer system Phosphate buffer system Ammonia buffer system KEY  Countertransport  Active transport  Exchange pump  Cotransport  Reabsorption  Secretion  Diffusion p. 1018

24. © 2012 Pearson Education, Inc. Figure 27-13b Kidney Tubules and pH Regulation KEY  Countertransport  Active transport  Exchange pump  Cotransport  Reabsorption  Secretion  Diffusion Production of ammonium ions and ammonia by the breakdown of glutamine Tubular fluid in lumen Glutaminase Carbon chain Glutamine p. 1018

25. © 2012 Pearson Education, Inc. Figure 27-13c Kidney Tubules and pH Regulation KEY  Countertransport  Active transport  Exchange pump  Cotransport  Reabsorption  Secretion  Diffusion The response of the kidney tubule to alkalosis Tubular fluid in lumen Carbonic anhydrase p. 1018

26. © 2012 Pearson Education, Inc. Figure 27-14 Interactions among the Carbonic Acid–Bicarbonate Buffer System and Compensatory Mechanisms in the Regulation of Plasma pH The response to acidosis caused by the addition of H  Addition of H  Start (carbonic acid) (bicarbonate ion) HH Other buffer systems absorb H  KIDNEYS Increased respiratory rate lowers P CO 2, effectively converting carbonic acid molecules to water. Lungs CO 2 CO 2  H 2 O Respiratory Response to Acidosis Secretion of H  H 2 CO 3 HCO 3    Na  BICARBONATE RESERVE NaHCO 3 Generation of HCO 3  Renal Response to Acidosis (sodium bicarbonate) Kidney tubules respond by (1) secreting H  ions, (2) removing CO 2, and (3) reabsorbing HCO 3  to help replenish the bicarbonate reserve. CARBONIC ACID-BICARBONATE BUFFER SYSTEM p. 1019

27. © 2012 Pearson Education, Inc. Figure 27-14b Interactions among the Carbonic Acid–Bicarbonate Buffer System and Compensatory Mechanisms in the Regulation of Plasma pH BICARBONATE RESERVE Removal of H  HH (carbonic acid) (bicarbonate ion) H 2 CO 3 HCO 3   Other buffer systems release H  Generation of H  Secretion of HCO 3  KIDNEYS H2OH2OCO 2  Lungs Respiratory Response to Alkalosis Decreased respiratory rate elevates P CO 2, effectively converting CO 2 molecules to carbonic acid. Renal Response to Alkalosis HCO 3  NaHCO 3 Na   (sodium bicarbonate) Kidney tubules respond by conserving H  ions and secreting HCO 3 . The response to alkalosis caused by the removal of H  Start CARBONIC ACID-BICARBONATE BUFFER SYSTEM p. 1019

28. © 2012 Pearson Education, Inc. Figure 27-15a Respiratory Acid–Base Regulation Responses to Acidosis Respiratory compensation: Stimulation of arterial and CSF chemo- receptors results in increased respiratory rate. Renal compensation: H  ions are secreted and HCO 3  ions are generated. Buffer systems other than the carbonic acid–bicarbonate system accept H  ions. Respiratory Acidosis Elevated P CO 2 results in a fall in plasma pH HOMEOSTASIS DISTURBED Hypoventilation causing increased P CO 2 HOMEOSTASIS Normal acid–base balance HOMEOSTASIS RESTORED Plasma pH returns to normal Decreased P CO 2 Decreased H  and increased HCO 3  Combined Effects Increased P CO 2 Respiratory acidosis p. 1021

29. © 2012 Pearson Education, Inc. Figure 27-15b Respiratory Acid–Base Regulation HOMEOSTASIS DISTURBED Hyperventilation causing decreased P CO 2 Respiratory Alkalosis Lower P CO 2 results in a rise in plasma pH Responses to Alkalosis Respiratory compensation: Inhibition of arterial and CSF chemoreceptors results in a decreased respiratory rate. Renal compensation: H  ions are generated and HCO 3  ions are secreted. Buffer systems other than the carbonic acid–bicarbonate system release H  ions. Respiratory alkalosis Decreased P CO 2 Combined Effects Increased P CO 2 Increased H  and decreased HCO 3  HOMEOSTASIS RESTORED Plasma pH returns to normal Normal acid–base balance HOMEOSTASIS p. 1021

30. © 2012 Pearson Education, Inc. Figure 27-16a Responses to Metabolic Acidosis Responses to Metabolic Acidosis Respiratory compensation: Stimulation of arterial and CSF chemo- receptors results in increased respiratory rate. Renal compensation: H  ions are secreted and HCO 3  ions are generated. Buffer systems accept H  ions. Metabolic Acidosis Elevated H  results in a fall in plasma pH HOMEOSTASIS DISTURBED Increased H  production or decreased H  excretion HOMEOSTASIS Normal acid–base balance HOMEOSTASIS RESTORED Plasma pH returns to normal Decreased H  and increased HCO 3  Decreased P CO 2 Combined Effects Increased H  ions Metabolic acidosis can result from increased acid production or decreased acid excretion, leading to a buildup of H  in body fluids. p. 1023

31. © 2012 Pearson Education, Inc. Figure 27-16b Responses to Metabolic Acidosis HOMEOSTASIS DISTURBED Bicarbonate loss; depletion of bicarbonate reserve Metabolic Acidosis Plasma pH falls because bicarbonate ions are unavailable to accept H  Responses to Metabolic Acidosis Respiratory compensation: Stimulation of arterial and CSF chemo- receptors results in increased respiratory rate. Renal compensation: H  ions are secreted and HCO 3  ions are generated. Buffer systems other than the carbonic acid–bicarbonate system accept H  ions. Metabolic acidosis can result from a loss of bicarbonate ions that makes the carbonic acid–bicarbonate buffer system incapable of preventing a fall in pH. Decreased HCO 3  ions Combined Effects Decreased P CO 2 Decreased H  and increased HCO 3  HOMEOSTASIS RESTORED Plasma pH returns to normal Normal acid–base balance HOMEOSTASIS p. 1023

32. © 2012 Pearson Education, Inc. Figure 27-17 Metabolic Alkalosis HOMEOSTASIS DISTURBED Loss of H  ; gain of HCO 3  Metabolic Acidosis Elevated HCO 3  results in a rise In plasma pH Responses to Metabolic Alkalosis Respiratory compensation: Stimulation of arterial and CSF chemoreceptors results in decreased respiratory rate. Renal compensation: H  ions are generated and HCO 3  Ions are secreted. Buffer systems other than the carbonic acid–bicarbonate system donate H  ions. Decreased H  ions, gain of HCO 3  ions Combined Effects Increased H  and decreased HCO 3  Increased P CO 2 HOMEOSTASIS RESTORED Plasma pH returns to normal Normal acid–base balance HOMEOSTASIS p. 1024

33. Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings © 2012 Pearson Education, Inc.

34. Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings © 2012 Pearson Education, Inc.

35. Figure 27-18 A Diagnostic Chart for Suspected Acid–Base Disorders Respiratory Acidosis P CO 2 increased (  50 mm Hg) Primary cause is hypoventilation Check P CO 2 Acidosis pH  7.35 (acidemia) Metabolic Acidosis P CO 2 normal or decreased Check HCO 3  Acute Respiratory Acidosis Chronic (compensated) Respiratory Acidosis Chronic (compensated) Metabolic Acidosis Acute Metabolic Acidosis P CO 2 normal P CO 2 decreased (  35 mm Hg) Examples: respiratory failure CNS damage pneumothorax Examples: emphysema asthma HCO 3  normalHCO 3  increased (  28 mEq/L) Reduction due to respiratory compensation Examples: diarrhea Examples: lactic acidosis ketoacidosis chronic renal failure Due to generation or retention of organic or fixed acids Due to loss of HCO 3  or to generation or ingestion of HCl NormalIncreased Check anion gap Check pH Suspected Acid–Base Disorder p. 1025

36. © 2012 Pearson Education, Inc. Figure 27-18 A Diagnostic Chart for Suspected Acid–Base Disorders Check pH Metabolic Alkalosis Respiratory Alkalosis P CO 2 increased (  45 mm Hg) P CO 2 decreased (  35 mm Hg) Alkalosis pH  7.45 (alkalemia) Check P CO 2 Primary cause is hyperventilation Check HCO 3  (HCO 3  will be elevated) Examples: vomiting loss of gastric acid Acute Respiratory Alkalosis Chronic (compensated) Respiratory Alkalosis Normal or slight decrease in HCO 3  Decreased HCO 3  (  24 mEq/L) Examples: fever panic attacks Examples: anemia CNS damage Suspected Acid–Base Disorder p. 1025

37. Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings © 2012 Pearson Education, Inc. p. 1025