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Acid base balance

  1. 1. ACID BASE BALANCE Dr Amith Sreedharan
  2. 2. DISCUSSION HEADINGS • BASICS • NORMAL PHYSIOLOGY • ABNORMALITIES • METABOLIC ACID BASE DISORDERS • RESPIRATORY ACID BASE DISORDERS • ALTERNATIVE CONCEPTS
  3. 3. • Acid Any compound which forms H⁺ ions in solution (proton donors) eg: Carbonic acid releases H⁺ ions • Base Any compound which combines with H⁺ ions in solution (proton acceptors) eg:Bicarbonate(HCO3⁻) accepts H+ ions
  4. 4. Acid–Base Balance Normal pH : 7.35-7.45 Acidosis Physiological state resulting from abnormally low plasma pH Alkalosis Physiological state resulting from abnormally high plasma pH Acidemia: plasma pH < 7.35  Alkalemia: plasma pH > 7.45
  5. 5. Henderson-Hasselbach equation (clinically relevant form) • pH = pKa + log([HCO3-]/.03xpCO2) • pH = 6.1 + log([HCO3-]/.03xpCO2) • Shows that pH is a function of the RATIO between bicarbonate and pCO2 • PCO₂ - ventilatory parameter (40 +/- 4) • HCO₃⁻ - metabolic parameter (22-26 mmol/L)
  6. 6. ACIDS • VOLATILE ACIDS:  Produced by oxidative metabolism of CHO,Fat,Protein  Average 15000-20000 mmol of CO₂ per day  Excreted through LUNGS as CO₂ gas • FIXED ACIDS (1 mEq/kg/day)  Acids that do not leave solution ,once produced they remain in body fluids Until eliminated by KIDNEYS Eg: Sulfuric acid ,phosphoric acid , Organic acids Are most important fixed acids in the body Are generated during catabolism of: amino acids(oxidation of sulfhydryl gps of cystine,methionine) Phospholipids(hydrolysis) nucleic acids
  7. 7. Response to ACID BASE challenge 1.Buffering 2. Compensation
  8. 8. Buffers First line of defence (> 50 – 100 mEq/day) Two most common chemical buffer groups – Bicarbonate – Non bicarbonate (Hb,protein,phosphate) Blood buffer systems act instantaneously Regulate pH by binding or releasing H⁺
  9. 9. Carbonic Acid–Bicarbonate Buffer System Carbon Dioxide  Most body cells constantly generate carbon dioxide  Most carbon dioxide is converted to carbonic acid, which dissociates into H+ and a bicarbonate ion Prevents changes in pH caused by organic acids and fixed acids in ECF  Cannot protect ECF from changes in pH that result from elevated or depressed 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
  10. 10. Acid–Base Balance The Carbonic Acid–Bicarbonate Buffer System
  11. 11. The Hemoglobin Buffer System CO2 diffuses across RBC membrane No transport mechanism required As carbonic acid dissociates Bicarbonate ions diffuse into plasma In exchange for chloride ions (chloride shift) • Hydrogen ions are buffered by hemoglobin molecules Is the only intracellular buffer system with an immediate effect on ECF pH Helps prevent major changes in pH when plasma PCO 2 is rising or falling
  12. 12. Phosphate Buffer System Consists of anion H2PO4- (a weak acid)(pKa-6.8) Works like the carbonic acid–bicarbonate buffer system Is important in buffering pH of ICF Limitations of Buffer Systems  Provide only temporary solution to acid– base imbalance  Do not eliminate H+ ions  Supply of buffer molecules is limited
  13. 13. Respiratory Acid-Base Control Mechanisms • When chemical buffers alone cannot prevent changes in blood pH, the respiratory system is the second line of defence against changes. Eliminate or Retain CO₂ Change in pH are RAPID Occuring within minutes PCO₂ ∞ VCO₂/VA
  14. 14. Renal Acid-Base Control Mechanisms • The kidneys are the third line of defence against wide changes in body fluid pH. – movement of bicarbonate – Retention/Excretion of acids – Generating additional buffers Long term regulator of ACID – BASE balance May take hours to days for correction
  15. 15. Renal regulation of acid base balance • Role of kidneys is preservation of body’s bicarbonate stores. • Accomplished by: – Reabsorption of 99.9% of filtered bicarbonate – Regeneration of titrated bicarbonate by excretion of: • Titratable acidity (mainly phosphate) • Ammonium salts
  16. 16. Renal reabsorption of bicarbonate • Proximal tubule: 70-90% • Loop of Henle: 10-20% • Distal tubule and collecting ducts: 4-7%
  17. 17. Factors affecting renal bicarbonate reabsorption • Filtered load of bicarbonate • Prolonged changes in pCO2 • Extracellular fluid volume • Plasma chloride concentration • Plasma potassium concentration • Hormones (e.g., mineralocorticoids, glucocorticoids)
  18. 18. • If secreted H+ ions combine with filtered bicarbonate, bicarbonate is reabsorbed • If secreted H+ ions combine with phosphate or ammonia, net acid excretion and generation of new bicarbonate occur
  19. 19. NET ACID EXCRETION • Hydrogen Ions Are secreted into tubular fluid along • Proximal convoluted tubule (PCT) • Distal convoluted tubule (DCT) • Collecting system
  20. 20. Titratable acidity • Occurs when secreted H+ encounter & titrate phosphate in tubular fluid • Refers to amount of strong base needed to titrate urine back to pH 7.4 • 40% (15-30 mEq) of daily fixed acid load • Relatively constant (not highly adaptable)
  21. 21. Ammonium excretion • Occurs when secreted H+ combine with NH3 and are trapped as NH4+ salts in tubular fluid • 60% (25-50 mEq) of daily fixed acid load • Very adaptable (via glutaminase induction)
  22. 22. Ammonium excretion • Large amounts of H+ can be excreted without extremely low urine pH because pKa of NH3/NH4+ system is very high (9.2)
  23. 23. Acid–Base Balance Disturbances Interactions among the Carbonic Acid–Bicarbonate Buffer System and Compensatory Mechanisms in the Regulation of Plasma pH.
  24. 24. Acid–Base Balance Disturbances decreased Interactions among the Carbonic Acid–Bicarbonate Buffer System and Compensatory Mechanisms in the Regulation of Plasma pH.
  25. 25. Four Basic Types of Imbalance • Metabolic Acidosis • Metabolic Alkalosis • Respiratory Acidosis • Respiratory Alkalosis
  26. 26. Acid Base Disorders Disorder pH [H+] Primary Secondary disturbance response Metabolic    [HCO3-]  pCO2 acidosis Metabolic    [HCO3-]  pCO2 alkalosis Respiratory    pCO2  [HCO3-] acidosis Respiratory    pCO2  [HCO3-] alkalosis
  27. 27. Metabolic Acidosis • Primary AB disorder • ↓HCO₃⁻ → ↓ pH • Gain of strong acid • Loss of base(HCO₃⁻)
  28. 28. ANION GAP CONCEPT • To know if Metabolic Acidosis due to  Loss of bicarbonate  Accumulation of non-volatile acids • Provides an index of the relative conc of plasma anions other than chloride,bicarbonate • *serum Na⁺ - (serum Cl⁻ + serum HCO₃⁻)+ • Unmeasured anions – unmeasured cations • 8 – 16 mEq/L (5 – 11,with newer techniques) • Mostly represent ALBUMIN
  29. 29. Concept of Anion Gap
  30. 30. Back
  31. 31. CAUSES OF METABOLIC ACIDOSIS (High anion gap)→(Normochloremic) LACTIC ACIDOSIS TOXINS KETOACIDOSIS Ethylene glycol Diabetic Methanol Alcoholic Salicylates Starvation Propylene glycol RENAL FAILURE (acute and chronic)
  32. 32. Normal anion gap(Hyperchloremic) MET.ACIDOSIS causes  Gastrointestinal  Drug-induced bicarbonate loss hyperkalemia (with renal A. Diarrhea insufficiency) B. External pancreatic or small-bowel A. Potassium-sparing diuretics (amiloride, drainage triamterene, spironolactone) C. Ureterosigmoidostomy, jejunal B. Trimethoprim loop, ileal loop C. Pentamidine D. Drugs D. ACE-Is and ARBs 1. Calcium chloride (acidifying agent) E. Nonsteroidal anti-inflammatory drugs F. Cyclosporine and tacrolimus 2. Magnesium sulfate (diarrhea) 3. Cholestyramine (bile acid diarrhea)  Other A. Acid loads (ammonium chloride, Renal acidosis hyperalimentation) A. Hypokalemia B. Loss of potential bicarbonate: ketosis 1. Proximal RTA (type 2) with ketone excretion 2. Distal (classic) RTA (type 1) C. Expansion acidosis (rapid saline administration) B. Hyperkalemia
  33. 33. URINE NET CHARGE/UAG Distinguish between hyperchloremic acidosis due to DIARRHEA RTA UNC= Na⁺+ K⁺- Cl⁻ • Provides an estimate of urinary NH₄⁺ production • Normal UAG = -25 to -50 Negative UAG – DIARRHEA(hyperchloremic acidosis) Positive UAG – RTA
  34. 34. “DELTA RATIO” / “GAP-GAP” FIG • Ratio between ↑in AG and ↓in bicarbonate • (Measured AG – 12):(24 – measured HCO₃⁻) • To detect another metabolic ACID BASE disorder along with HAGMA (nagma/met.alkalosis) • HAGMA(NORMOCHLOREMIC ACIDOSIS) :- RATIO = 1 HYPERCHLOREMIC ACIDOSIS (NAGMA):- RATIO < 1 In DKA pts,after therapy with NS • Met.acidosis with Met.alkalosis :- RATIO > 1 Use of NG suction and DIURETICS in met.acidosis pt
  35. 35. Compensation for Metabolic acidosis • H+ buffered by ECF HCO3- & Hb in RBC; Plasma Pr and Pi: negligible role (sec-min) • Hyperventilation – to reduce PCO₂ • ↓pH sensed by central and peripheral chemoreceptors • ↑ in ventilation starts within minutes,well advanced at 2 hours • Maximal compensation takes 12 – 24 hours • Expected PCO₂ calculated by WINTERS’ FORMULA EXP.PCO₂ =1.5 X (ACTUAL HCO₃⁻ )+8 +/- 2 mmHg Limiting value of compensation: PCO₂ = 8-10mmHg Quick rule of thumb :PCO₂ = last 2 digits of pH
  36. 36. Acid–Base Balance Disturbances . Responses to Metabolic Acidosis
  37. 37. Metabolic acidosis  Symptoms are specific and a result of the underlying pathology • Respiratory effects:  Hyperventilation • CVS:  ↓ myocardial contractility  Sympathetic over activity  Resistant to catecholamines • CNS:  Lethargy,disorientation,stupor,muscle twitching,COMA, CN palsies • Others : hyperkalemia
  38. 38. Metabolic Alkalosis ↑ pH due to ↑HCO₃⁻ or ↓acid • Initiation process :  ↑in serum HCO₃⁻  Excessive secretion of net daily production of fixed acids • Maintenance:  ↓HCO₃⁻ excretion or ↑ HCO₃⁻ reclamation  Chloride depletion  Pottasium depletion  ECF volume depletion  Magnesium depletion
  39. 39. CAUSES OF METABOLIC ALKALOSIS I. Exogenous HCO3 − loads A. Acute alkali administration B. Milk-alkali syndrome II. Gastrointestinal origin 1. Vomiting 2. Gastric aspiration 3. Congenital chloridorrhea 4. Villous adenoma III. Renal origin 1. Diuretics 2. Posthypercapnic state 3. Hypercalcemia/hypoparathyroidism 4. Recovery from lactic acidosis or ketoacidosis 5. Nonreabsorbable anions including penicillin, carbenicillin 6. Mg2+ deficiency 7. K+ depletion
  40. 40. Chloride responsive alkalosis  Low urinary chloride concentration(<15 meq/L) Gastric acid loss Diuretic therapy Volume depletion Renal compensation for hypercapnea Chloride resistant alkalosis  Elevated urinary chloride (>25 meq/L) 1⁰ mineralocorticoid excess Severe pottasium depletion  A/W volume expansion
  41. 41. Compensation for Metabolic Alkalosis • Respiratory compensation: HYPOVENTILATION ↑PCO₂=0.6 mm  pCO2 per 1.0 mEq/L ↑HCO3- • Maximal compensation: PCO₂ 55 – 60 mmHg • Hypoventilation not always found due to Hyperventilation due to pain due to pulmonary congestion due to hypoxemia(PO₂ < 50mmHg)
  42. 42. Acid–Base Balance Disturbances . Metabolic Alkalosis
  43. 43. Metabolic Alkalosis  Decreased myocardial contractility  Arrythmias  ↓ cerebral blood flow  Confusion  Mental obtundation  Neuromuscular excitability • Hypoventilation  pulmonary micro atelectasis  V/Q mismatch(alkalosis inhibits HPV)
  44. 44. Contraction Alkalosis • Loss of HCO₃⁻ poor, chloride rich ECF • Contraction of ECF volume • Original HCO₃⁻ dissolved in smaller volume • ↑HCO₃⁻ concentration • Eg : Loop diuretics/Thiazides in a generalised edematous pt.
  45. 45. Respiratory Acidosis • ↑ PCO₂ → ↓pH • Acute(< 24 hours) • Chronic(>24 hours)
  46. 46. RESPIRATORY ACIDOSIS - CAUSES CNS DEPRESSION  DRUGS:Opiates,sedatives,anaesthetics  OBESITY HYPOVENTILATION SYNDROME  STROKE NEUROMUSCULAR DISORDERS  NEUROLOGIC:MS,POLIO,GBS,TETANUS,BOTULISM, HIGH CORD LESIONS  END PLATE:MG,OP POISONING,AG TOXICITY  MUSCLE:↓K⁺,↓PO₄,MUSCULAR DYSTROPHY AIRWAY OBSTRUCTION  COPD,ACUTE ASPIRATION,LARYNGOSPASM
  47. 47. CONT.. CHEST WALL RESTRICTION  PLEURAL: Effusions, empyema,pneumothorax,fibrothorax  CHEST WALL: Kyphoscoliosis, scleroderma,ankylosing spondylitis,obesity SEVERE PULMONARY RESTRICTIVE DISORDERS  PULMONARY FIBROSIS  PARENCHYMAL INFILTRATION: Pneumonia, edema ABNORMAL BLOOD CO₂ TRANSPORT  DECREASED PERFUSION: HF,cardiac arrest,PE  SEVERE ANEMIA  ACETAZOLAMIDE-CA Inhibition  RED CELL ANION EXCHANGE: Loop diuretics, salicylates, NSAID
  48. 48. Compensation in Respiratory Acidosis Acute resp.acidosis:  Mainly due to intracellular buffering(Hb,Pr,PO₄) HCO₃⁻ ↑ = 1mmol for every 10 mmHg ↑ PCO₂  Minimal increase in HCO₃⁻  pH change = 0.008 x (40 - PaCO₂) Chronic resp.acidosis  Renal compensation (acidification of urine & bicarbonate retention) comes into action HCO₃⁻ ↑= 3.5 mmol for every 10 mm Hg ↑PCO₂  pH change = 0.003 x (40 - PaCO₂)  Maximal response : 3 - 4 days
  49. 49. Acid–Base Balance Disturbances Respiratory Acid–Base Regulation.
  50. 50. • RS:  Stimulation of ventilation ( tachypnea)  dyspnea • CNS:  ↑cerebral blood flow→ ↑ICT  CO₂ NARCOSIS (Disorientation,confusion,headache,lethargy)  COMA(arterial hypoxemia,↑ICT,anaesthetic effect of ↑ PCO₂ > 100mmHg) • CVS:  tachycardia,bounding pulse • Others:  peripheral vasodilatation(warm,flushed,sweaty)
  51. 51. Post hypercapnic alkalosis • In chronic resp.acidosis • Renal compensation → ↑HCO₃⁻ • If the pt intubated and mechanical ventilated • PCO₂ rapidly corrected • Plasma HCO₃⁻ doesn’t return to normal rapidly • HCO₃⁻ remains high
  52. 52. Respiratory Alkalosis • Most common AB abnormality in critically ill • ↓PCO₂ → ↑pH • 1⁰ process : hyperventilation • Acute: PaCO₂ ↓,pH-alkalemic • Chronic: PaCO₂↓,pH normal / near normal
  53. 53. CAUSES OF RESPIRATORY ALKALOSIS A. Central nervous system C. Drugs or hormones stimulation 1. Pregnancy, progesterone 1. Pain 2. Salicylates 2. Anxiety, psychosis 3. Cardiac failure 3. Fever D. Stimulation of chest receptors 4. Cerebrovascular accident 1. Hemothorax 5. Meningitis, encephalitis 2. Flail chest 3. Cardiac failure 6. Tumor 4. Pulmonary embolism 7. Trauma E. Miscellaneous B. Hypoxemia or tissue 1. Septicemia hypoxia 2. Hepatic failure 1. High altitude 3. Mechanical ventilation 2. Septicemia 4. Heat exposure 3. Hypotension 5. Recovery from metabolic 4. Severe anemia acidosis
  54. 54. Compensation for respiratory Alkalosis Acute resp.alkalosis:  Intracellular buffering response-slight decrease in HCO₃⁻  Start within 10 mins ,maximal response 6 hrs  Magnitude:2 mmol/L↓HCO₃⁻ for 10 mmHg↓PCO₂  LIMIT: 12-20 mmol/L (avg=18) Chronic resp.alkalosis:  Renal compensation (acid retention,HCO₃⁻ loss)  Starts after 6 hours, maximal response 2- 3 days  Magnitude : 5mmol/L ↓HCO₃⁻ for 10mmHg ↓PCO₂  LIMIT: 12-15 mmol/L HCO₃⁻
  55. 55. Acid–Base Balance Disturbances Respiratory Acid–Base Regulation.
  56. 56. Respiratory alkalosis • CNS:  ↑ neuromuscular irritability(tingling,circumoral numbness)  Tetany  ↓ ICT(cerebral VC)  ↓CBF(4% ↓ CBF per mmHg ↓PCO₂)  Light headedness,confusion • CVS:  CO& SBP ↑ (↑ SVR,HR)  Arrythmias  ↓ myocardial contractility • Others:  Hypokalemia,hypophosphatemia  ↓Free serum calcium  Hyponatremia,hypochloremia
  57. 57. Acid Base Disorders Primary disorder Compensatory response Metabolic acidosis PCO₂=1.5 X (HCO₃⁻) + 8 +/₋ 2*Winter’s formula+ Metabolic alkalosis 0.6 mm  pCO2 per 1.0 mEq/L  HCO3- Acute respiratory acidosis 1 mEq/L  HCO3- per 10 mm  pCO2 Chronic respiratory acidosis 3.5 mEq/L  HCO3- per 10 mm  pCO2 Acute respiratory alkalosis 2 mEq/L  HCO3- per 10 mm  pCO2 Chronic respiratory alkalosis 5 mEq/L  HCO3- per 10 mm  pCO2
  58. 58. STRONG ION APPROACH • Metabolic parameter divided into 2 components “STRONG” acids and bases  Electrolytes, lactate,acetoacetate,sulfate “WEAK” buffer molecules  Serum proteins and phosphate • pH calculated on the basis of 3 simple assumptions  Total concentrations of each of the ions and acid base pairs is known and remains unchanged  Solution remains electroneutral  Dissociation constants of each of the buffers are known • Both pH and bicarbonate are dependent variables that can be calculated from the concentrations of “STRONG” and “WEAK” electrolytes and PCO₂
  59. 59. STRONG ION DIFFERENCE (SID) • STRONG CATIONS – STRONG ANIONS • Decrease in SID → Acidification of PLASMA • Explains – NS induced ACIDOSIS • ADV: Estimate of H⁺ conc more accurate than Henderson Hasselbalch equation. • DIS ADV:Complex nature of equations,increased parameters limit clinical application
  60. 60. BASE EXCESS/DEFICIT • Base excess and base deficit are terms applied to an analytical method for determination of the appropriateness of responses to disorders of acid-base metabolism • by measuring blood pH against ambient PCO2 and against a PCO2 of 40 mmHg • deficit is expressed as the number of mEq of bicarbonate needed to restore the serum bicarbonate to 25 mEq/L at a PCO₂ of 40 mmHg compared with that at the ambient PCO₂ • misleading in chronic respiratory alkalosis or acidosis • physiological evaluation of the patient be the mode of analysis of acid-base disorders rather than an emphasis on derived formulae
  61. 61. ACID BASE NORMOGRAM
  62. 62. MIXED ACID BASE DISORDER Diagnosed by combination of clinical assessment, application of expected compensatory responses , assessment of the anion gap, and application of principles of physiology. Respiratory acidosis and alkalosis never coexist Metabolic disorders can coexist Eg: lactic acidosis/DKA with vomiting Metabolic and respiratory AB disorders can coexist Eg: salicylate poisoning (met.acidosis + resp.alkalosis)
  63. 63. THANK YOU LIFE IS A STRUGGLE, NOT AGAINST SIN, NOT AGAINST MONEY POWER.. BUT AGAINST HYDROGEN IONS . H.L.MENCKEN
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