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![Human Acid-base Homeostasis
• Tight regulation:
• CO2 tension
• by respiratory excretion (of volatile acids)
• Plasma bicarbonate [HCO3
-]
• By renal HCO3
- reabsorption and
• Elimination of protons produced by metabolism
• pH is determined by CO2 tension and [HCO3
-]](https://image.slidesharecdn.com/acidbasebalancekabsom-200305112811/75/Acid-base-balance-in-surgery-2-2048.jpg)
![Normal Values
• [HCO3
-] ~ 24 mM
• PaCO2 = 38 torr
• pH ~ 7.42
• Plasma HCO3
- regulation by
• reclaiming filtered HCO3
- and
• generating new HCO3
- (carboanhydrase)
• ( to replace the lost internally titrating metabolic acid and
externally from the GI tract)
• Production of 1 mmol of acid/kg body weight per
day (60 kg=60 mmol/day)](https://image.slidesharecdn.com/acidbasebalancekabsom-200305112811/75/Acid-base-balance-in-surgery-7-2048.jpg)
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Acid base balance in surgery
- 1. Acid -Base balance Drmugarura Robert
- 2. Human Acid-base Homeostasis •Tight regulation: • CO2 tension • by respiratory excretion (of volatile acids) • Plasma bicarbonate [HCO3 -] • By renal HCO3 - reabsorption and • Elimination of protons produced by metabolism • pH is determined by CO2 tension and [HCO3 -]
- 3. Acid base balance •Normal ranges PH 7.35 to 7.45 • Alkalosis PH > 7.45 • Acidosis PH < 7.35 • Disorders of acid base balance can be : • Respiratory • Metabolic
- 4. Body acids • Fixedacids • SO4, PO4 , lactic acid, fatty acids, ketone bodies, • Are products of metabolism- 1 mmol of fixed acid/kg body weight per day (60 kg=60 mmol/day) • Volatile: H2CO3 • Product of respiration- external
- 5. Acidosis • Increased PCO2 •Increased A tot- (hyperphosphatemia, hyperproteinemia)
- 6. Alkalosis • Decreased PCO2 •decreased A tot- (hypophosphatemia, hypoproteinemia
- 7. Normal Values • [HCO3 -]~ 24 mM • PaCO2 = 38 torr • pH ~ 7.42 • Plasma HCO3 - regulation by • reclaiming filtered HCO3 - and • generating new HCO3 - (carboanhydrase) • ( to replace the lost internally titrating metabolic acid and externally from the GI tract) • Production of 1 mmol of acid/kg body weight per day (60 kg=60 mmol/day)
- 8. .. For optimal functioningof cells Acids and bases in the body must be in balance.
- 9. Body pH Balance •Chemical blood buffers: • Physiological Buffer Systems • Lungs, • Cells, • Kidneys
- 10. Chemical Buffer Systems •Chemical buffer: system of one or more compounds that act to resist pH changes when strong acid or base is added 1. Bicarbonate buffer system 2. Phosphate buffer system 3. Protein buffer system
- 11. Bicarbonate Buffer System •Mixture of H2CO3 (weak acid) and salts of HCO3 – (e.g., NaHCO3, a weak base) • Buffers ICF and ECF • The only important ECF buffer
- 12. Bicarbonate Buffer System •If strong acid is added: • HCO3 – ties up H+ and forms H2CO3 • HCl + NaHCO3 H2CO3 + NaCl • pH decreases only slightly, unless all available HCO3 – (alkaline reserve) is used up • HCO3 – concentration is closely regulated by the kidneys
- 13. Bicarbonate Buffer System •If strong base is added • It causes H2CO3 to dissociate and donate H+ • H+ ties up the base (e.g. OH–) • NaOH + H2CO3 NaHCO3 + H2O • pH rises only slightly • H2CO3 supply is almost limitless (from CO2 released by respiration) and is subject to respiratory controls
- 14. Phosphate Buffer System •Action is nearly identical to the bicarbonate buffer • Components are sodium salts of: • Dihydrogen phosphate (H2PO4 –), a weak acid • Monohydrogen phosphate (HPO4 2–), a weak base • Effective buffer in urine and ICF, where phosphate concentrations are high
- 15. Protein Buffer System •Intracellular proteins are the most plentiful and powerful buffers; plasma proteins are also important • Protein molecules are amphoteric (can function as both a weak acid and a weak base) • When pH rises, organic acid or carboxyl (COOH) groups release H+ • When pH falls, NH2 groups bind H+
- 16. Physiological Buffer Systems •Respiratory and renal systems • Act more slowly than chemical buffer systems • Have more capacity than chemical buffer systems
- 17. Respiratory Regulation ofH+ • Respiratory system eliminates CO2 • A reversible equilibrium exists in the blood: • CO2 + H2O H2CO3 H+ + HCO3 – • During CO2 unloading the reaction shifts to the left (and H+ is incorporated into H2O) • During CO2 loading the reaction shifts to the right (and H+ is buffered by proteins)
- 18. Total Acid- baseMetabolism Henderson-Hasselbalch 1909,1916 HCO3 - • pH = pK + log ------------ PaCO2 Result of Metabolic and Respiratory Interplay Primary Respiratory Disorders Altered by Respiratory Compensation for Metabolic Disorders Metabolic comp. Respiratory component Altered by Buffering Primarily Altered in Metabolic Disorders
- 19. Respiratory Regulation ofH+ • Hypercapnia activates medullary chemoreceptors • Rising plasma H+ activates peripheral chemoreceptors • More CO2 is removed from the blood • H+ concentration is reduced
- 20. Respiratory Regulation ofH+ • Alkalosis depresses the respiratory center • Respiratory rate and depth decrease • H+ concentration increases • Respiratory system impairment causes acid-base imbalances • Hypoventilation respiratory acidosis • Hyperventilation respiratory alkalosis
- 21. Acid-Base Balance • Chemicalbuffers cannot eliminate excess acids or bases from the body • Lungs eliminate volatile carbonic acid by eliminating CO2 • Kidneys eliminate other fixed metabolic acids (phosphoric, uric, and lactic acids and ketones) and prevent metabolic acidosis
- 22. Renal Mechanisms ofAcid-Base Balance • Most important renal mechanisms • Conserving (reabsorbing) or generating new HCO3 – • Excreting HCO3 – • Generating or reabsorbing one HCO3 – is the same as losing one H+ • Excreting one HCO3 – is the same as gaining one H+
- 23. Renal Mechanisms ofAcid-Base Balance • Renal regulation of acid-base balance depends on secretion of H+ • H+ secretion occurs in the PCT and in collecting duct type A intercalated cells: • The H+ comes from H2CO3 produced in reactions catalyzed by carbonic anhydrase inside the cells • See Steps 1 and 2 of the following figure
- 24. Figure 26.12 1 CO2combines with water within the tubule cell, forming H2CO3. 2 H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3 –). 3a H+ is secreted into the filtrate. 3b For each H+ secreted, a HCO3 – enters the peritubular capillary blood either via symport with Na+ or via antiport with CI–. 4 Secreted H+ combines with HCO3 – in the filtrate, forming carbonic acid (H2CO3). HCO3 – disappears from the filtrate at the same rate that HCO3 – (formed within the tubule cell) enters the peritubular capillary blood. 5 The H2CO3 formed in the filtrate dissociates to release CO2 and H2O. 6 CO2 diffuses into the tubule cell, where it triggers further H+ secretion. * CA CO2 CO2 + H2O 2K+2K+ * Na+ Na+ 3Na+3Na+ Tight junction H2CO3 H2CO3 PCT cell NucleusFiltrate in tubule lumen Cl–Cl–HCO3 – + Na+ HCO3 – H2O CO2 H+ H+ HCO3 – HCO3 – HCO3 – ATPase ATPase Peri- tubular capillary 1 2 4 5 6 3a 3b Primary active transport Simple diffusion Secondary active transport Carbonic anhydrase Transport protein
- 25. Reabsorption of Bicarbonate •Tubule cell luminal membranes are impermeable to HCO3 – • CO2 combines with water in PCT cells, forming H2CO3 • H2CO3 dissociates • H+ is secreted, and HCO3 – is reabsorbed into capillary blood • Secreted H+ unites with HCO3 – to form H2CO3 in filtrate, which generates CO2 and H2O • HCO3 – disappears from filtrate at the same rate that it enters the peritubular capillary blood
- 26. Figure 26.12 1 CO2combines with water within the tubule cell, forming H2CO3. 2 H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3 –). 3a H+ is secreted into the filtrate. 3b For each H+ secreted, a HCO3 – enters the peritubular capillary blood either via symport with Na+ or via antiport with CI–. 4 Secreted H+ combines with HCO3 – in the filtrate, forming carbonic acid (H2CO3). HCO3 – disappears from the filtrate at the same rate that HCO3 – (formed within the tubule cell) enters the peritubular capillary blood. 5 The H2CO3 formed in the filtrate dissociates to release CO2 and H2O. 6 CO2 diffuses into the tubule cell, where it triggers further H+ secretion. * CA CO2 CO2 + H2O 2K+2K+ * Na+ Na+ 3Na+3Na+ Tight junction H2CO3 H2CO3 PCT cell NucleusFiltrate in tubule lumen Cl–Cl–HCO3 – + Na+ HCO3 – H2O CO2 H+ H+ HCO3 – HCO3 – HCO3 – ATPase ATPase Peri- tubular capillary 1 2 4 5 6 3a 3b Primary active transport Simple diffusion Secondary active transport Carbonic anhydrase Transport protein
- 27. Generating New BicarbonateIons • Two mechanisms in PCT and type A intercalated cells • Generate new HCO3 – to be added to the alkaline reserve • Both involve renal excretion of acid (via secretion and excretion of H+ or NH4 +
- 28. Excretion of BufferedH+ • Dietary H+ must be balanced by generating new HCO3 – • Most filtered HCO3 – is used up before filtrate reaches the collecting duct
- 29. Excretion of BufferedH+ • Intercalated cells actively secrete H+ into urine, which is buffered by phosphates and excreted • Generated “new” HCO3 – moves into the interstitial space via a cotransport system and then moves passively into peritubular capillary blood
- 30. Figure 25.13 Active transport Passive transport Peri- tubular capillary 2 4 4 3 31 1 243 Filtrate in tubule lumen Transcellular Paracellular Paracellular Tight junction Lateral intercellular space Capillary endothelial cell Luminal membrane Solutes H2O Tubule cell Interstitial fluid Transcellular Basolateral membranes 1 Transport across the luminal membrane. 2 Diffusion through the cytosol. 4 Movement through the interstitial fluid and into the capillary. 3 Transport across the basolateral membrane. (Often involves the lateral intercellular spaces because membrane transporters transport ions into these spaces.) Movement via the transcellular route involves: The paracellular route involves: • Movement through leaky tight junctions, particularly in the PCT.
- 31. Ammonium Ion Excretion •Involves metabolism of glutamine in PCT cells • Each glutamine produces 2 NH4 + and 2 “new” HCO3 – • HCO3 – moves to the blood and NH4 + is excreted in urine
- 32. Figure 26.14 Nucleus PCT tubulecells Filtrate in tubule lumen Peri- tubular capillary NH4 + out in urine 2NH4 + Na+ Na+ Na+ Na+ Na+ 3Na+ 3Na+ Glutamine GlutamineGlutamine Tight junction Deamination, oxidation, and acidification (+H+) 2K+2K+ NH4 + HCO3 – 2HCO3 – HCO3 – (new) ATPase 1 PCT cells metabolize glutamine to NH4 + and HCO3 –. 2a This weak acid NH4 + (ammonium) is secreted into the filtrate, taking the place of H+ on a Na+- H+ antiport carrier. 2b For each NH4 + secreted, a bicarbonate ion (HCO3 –) enters the peritubular capillary blood via a symport carrier. 3 The NH4 + is excreted in the urine. Primary active transport Simple diffusion Secondary active transport Transport protein 1 2a 2b 3
- 33. Bicarbonate Ion Secretion •When the body is in alkalosis, type B intercalated cells • Secrete HCO3 – • Reclaim H+ and acidify the blood
- 34. Bicarbonate Ion Secretion •Mechanism is the opposite of the bicarbonate ion reabsorption process by type A intercalated cells • Even during alkalosis, the nephrons and collecting ducts excrete fewer HCO3 – than they conserve
- 35. Abnormalities of Acid-BaseBalance • Respiratory acidosis and alkalosis • Metabolic acidosis and alkalosis
- 36. Respiratory Acidosis andAlkalosis • The most important indicator of adequacy of respiratory function is PCO2 level (normally 35–45 mm Hg) • PCO2 above 45 mm Hg respiratory acidosis • Most common cause of acid-base imbalances • Due to decrease in ventilation or gas exchange • Characterized by falling blood pH and rising PCO2
- 37. Respiratory Acidosis andAlkalosis • PCO2 below 35 mm Hg respiratory alkalosis • A common result of hyperventilation due to stress or pain
- 38. Metabolic Acidosis andAlkalosis • Any pH imbalance not caused by abnormal blood CO2 levels • Indicated by abnormal HCO3 – levels
- 39. Metabolic Acidosis andAlkalosis • Causes of metabolic acidosis • Ingestion of too much alcohol ( acetic acid) • Excessive loss of HCO3 – (e.g., persistent diarrhea) • Accumulation of lactic acid, shock, ketosis in diabetic crisis, starvation, and kidney failure
- 40. Metabolic Acidosis andAlkalosis • Metabolic alkalosis is much less common than metabolic acidosis • Indicated by rising blood pH and HCO3 – • Caused by vomiting of the acid contents of the stomach or by intake of excess base (e.g., antacids)
- 41. Effects of Acidosisand Alkalosis • Blood pH below 7 depression of CNS coma death • Blood pH above 7.8 excitation of nervous system muscle tetany, extreme nervousness, convulsions, respiratory arrest
- 42. Respiratory and RenalCompensations • If acid-base imbalance is due to malfunction of a physiological buffer system, the other one compensates • Respiratory system attempts to correct metabolic acid-base imbalances • Kidneys attempt to correct respiratory acid-base imbalances
- 43. Respiratory Compensation • Inmetabolic acidosis • High H+ levels stimulate the respiratory centers • Rate and depth of breathing are elevated • Blood pH is below 7.35 and HCO3 – level is low • As CO2 is eliminated by the respiratory system, PCO2 falls below normal
- 44. Respiratory Compensation • Respiratorycompensation for metabolic alkalosis is revealed by: • Slow, shallow breathing, allowing CO2 accumulation in the blood • High pH (over 7.45) and elevated HCO3 – levels
- 45. Renal Compensation • Hypoventilationcauses elevated PCO2 • (respiratory acidosis) • Renal compensation is indicated by high HCO3 – levels • Respiratory alkalosis exhibits low PCO2 and high pH • Renal compensation is indicated by decreasing HCO3 – levels
- 46. Developmental Aspects • Infantshave proportionately more ECF than adults until about 2 years of age • Problems with fluid, electrolyte, and acid-base balance are most common in infancy, 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, especially during the first month
- 47. Developmental Aspects • Atpuberty, sexual differences in body water content arise as males develop greater muscle mass • In old age, total body water often decreases • Homeostatic mechanisms slow down with age • Elders may be unresponsive to thirst clues and are at risk of dehydration