Acid-Base Disorders

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  • 1. • CSN Vittal
  • 2. • pH : 7.35 – 7.45 • PaCO2 : 35 – 45 mm Hg • PaO2 : > 70 mm Hg • HCO3- : 22 – 26 mEq/L • BE : -2.0 to +2.0 mEq/L
  • 3. • Depends on Acid : Base • Proportional to HCO3- / H2CO3 • pH change to HCO3- is metabolic • pH change to H2CO3 (CO2) is respiratory
  • 4. • Difference between patient’s actual buffering capacity and normal buffering capacity • Normal Values : +/- 2.0 mEq/L • Follows changes in HCO3-
  • 5. 1. Carbon dioxide (since CO2 and H2O form HCO3-, and H+ in the presence of carbonic anhydrase) 2. Production of nonvolatile acids from the metabolism of proteins and other organic molecules 3. Loss of bicarbonate in faeces or urine 4. Intake of acids or acid precursors 1. Use of hydrogen ions in the metabolism of various organic anions 2. Loss of acid in the vomitus or urine
  • 6. • Consider the history • Look for clues on physical exam • Examine the electrolytes – PCO2 – Potassium – Anion Gap • Review other laboratory data • Analyze the arterial blood gas
  • 7. • Loose Stools and decreased Intake • Polyphagia, Polydipsia of DM • History of Renal Insufficiency • Possibilty of Poisoning in Toddlers • Fever and Increasing Sickness • Any signs of CNS Disorder • Any Medication History
  • 8. • Any Signs of Sepsis • Any Signs of Dehydration • Any Signs of Meningeal irritation • Any Signs of Addison’s Disease • Any Signs of Neuromuscular Disease
  • 9. 5 Step Approach 1. 2. 3. 4. pH: Normal, acid or alkaline? Respiratory component – Is it like pH? Metabolic component – Is SBE like pH? Magnitude of change – minor, moderate or major? 5. Recognizing compensation
  • 10. Step 1 Acidemic or Alkalotic? • • Acidemic Alkalotic : pH < 7.35 : pH > 7.45 A normal pH does not rule out acid base disorder
  • 11. Step 2 Respiratory Component : PCO2 If the respiratory change is like the pH, i.e., both acid, then the cause is respiratory The exception : when the metabolic component is also acid -> both are contributing to the acid pH. If the PCO2 is not like the pH, i.e., the PCO2 is low (alkaline), then the primary problem is not respiratory; the low PCO2 is a compensation for the metabolic acidosis.
  • 12. Step 3 Metabolic Component : SBE If the Standard Base Excess (SBE) is the component which is like the pH, i.e., both acid (a negative base excess), then the cause is metabolic. The exception, - is when the respiratory component is also acid; then both contribute to the acid pH. If the SBE is not like the pH, i.e., the SBE is alkaline, then the primary problem is not metabolic; the high SBE is a compensation for the respiratory acidosis.
  • 13. Step 4 Magnitude of Disturbance Just try to judge minor, moderate, or major, for clinical comment. Whenever the pH is normal, i.e., pH = 7.4. then the PCO2 and the SBE are equal and opposite. The slope for BE / PCO2 when pH = 7.4 gives us this ratio: 3 units of change in SBE = 5 mm Hg change in PCO2. Adjective PCO2 mmHg SBE mEq/L Severe <18 <13 Marked 18 to 25 13 to 9 Moderate 25 to 30 9 to 6 Mild 30 to 34 6 to 4 Minimal 34 to 37 4 to 2 Normal Normal 37 to 43 2 to -2 Acidosis Minimal 43 to 46 -2 to -4 Mild 46 to 50 -4 to -6 Moderate 50 to 55 -6 to -9 Marked 55 to 62 -9 to -13 Severe > 62 to <-13 Alkalosis
  • 14. Step 5 Recognizing compensation • If a pt. with a respiratory problem has a high PCO2, e.g., 60 mmHg (raised by 20mmHg) then for "complete compensation" the SBE would have to be about 12 (using the 5 to 3 ratio given above). • If the SBE were zero = "no compensation" typical of an acute process of recent onset. Most likely - the patient is somewhere in the middle (SBE = 6 mEq/L) which is typical for "compensation for chronic respiratory acidosis”.
  • 15. Step 5 Recognizing compensation Inverse example: • if a patient with a metabolic problem has a low SBE, e.g., -12, then the PCO2 would have to be reduced by hyperventilation to about 20 mmHg to achieve "complete compensation". • If the PCO2 were still normal then there would be "no compensation". Again, far the most likely, the patient is somewhere in the middle (30 mmHg) which is typical for "compensation for metabolic acidosis".
  • 16. Logical Approach to an Acid pH 1. Are the pH and the PCO2 both acid? If so the PCO2 contributes to the condition. 2. If not (i.e., PCO2 is alkaline) then the metabolic component is the cause and the PCO2 is compensatory. 3. Is either PCO2 or SBE normal? Because, if so, there is no compensation and you have a pure acidosis: (pure respiratory acidosis occurs fairly frequently, metabolic rarely) 1. To be typical the compensation must lie roughly half way between no compensation and complete compensation use the rule 3 mEq/L = 5 mmHg to work out complete compensation. 2. If both components are acid, you don't have a typical single condition, you have a combined metabolic and respiratory acidosis.
  • 17. Example A pH = 7.2, PCO2 = 60 mmHg, SBE = 0 mEq/L • Overall change is acid. • Respiratory change is also acid - therefore contributing to the acidosis. • SBE is normal - no metabolic compensation. • Therefore, pure respiratory acidosis. • Typical of acute respiratory depression. • Magnitude: marked respiratory acidosis
  • 18. Example B pH = 7.35, PCO2 = 60 mmHg, SBE = 7 mEq/L • Overall change is slightly acid. • Respiratory change is also acid - therefore contributing to the acidosis. • Metabolic change is alkaline - therefore compensatory. • The respiratory acidosis is 20 mmHg on the acid side of normal (40). To completely balance plus 20 would require 20 * 3 / 5 = 12 mEq/L SBE • The actual SBE is 7 mEq/L, which is roughly half way between 0 and 12, i.e., a typical metabolic compensation. • Magnitude: marked respiratory acidosis with moderate metabolic compensation
  • 19. Example C pH = 7.15, PCO2 = 60 mmHg, SBE = - 6 mEq/L • Overall change is acid. • Respiratory change is acid - therefore contributing to the acidosis. • Metabolic change is also acid - therefore combined acidosis. • The components are pulling in same direction - neither can be compensating for the other • Magnitude: marked respiratory acidosis and mild metabolic acidosis
  • 20. Example D pH= 7.30, PCO2 = 30 mmHg, SBE = -10 mEq/L • • • • • • • Overall change is acid. Resp. change is alkaline - therefore NOT contributing to the acidosis. Metabolic change is acid - therefore responsible for the acidosis. The components are pulling in opposite directions. SBE is the acid component so it is primarily a metabolic problem with some respiratory compensation The metabolic acidosis is 10 mEq/L on the acid side of normal (0). To completely balance 10 would require 10 * 5 / 3 = 17 mmHg respiratory alkalosis (= 23 mmHg) The actual PCO2 is 30 mEq/L which is roughly half way between 23 and 40, i.e., a typical respiratory compensation.. Magnitude: marked metabolic acidosis with mild respiratory compensation.
  • 21. Respir ator y Acidosis  Acute  The PaCO2 is elevated above the upper limit of the reference range (i.e., > 45 mm Hg) with an accompanying acidemia (i.e., pH < 7.35).  Chronic  The PaCO2 is elevated above the upper limit of the reference range, with a normal or near-normal pH secondary to renal compensation and an elevated serum bicarbonate (i.e., HCO3- > 30 mEq/L.)
  • 22. Respir ator y Disturbances  Is it Acute or Chronic ? Respiratory Acidosis Respiratory Alkalosis Acute: Acute: pH decrease pH Increase = 0.008 X (PaCO2 – 40) = 0.008 X (PaCO2 – 40) Chronic: Chronic: pH decrease pH Increase = 0.003 X (PaCO2 – 40) = 0.003 X (PaCO2 – 40)
  • 23. Respirator y Acidosis Acute Abrupt failure of ventilation,  PaCO2  Neuromuscular disorders   CNS Depression Brain stem Injury  Musculoskeletal Disorders  GBS  Myasthenia  Airway Obstructive Disease     Asthma Foreign Body Laryngeal Edema Pulmonary Embolism  Drugs  Sedatives  Barbiturates
  • 24. Respirator y Acidosis Chronic  COPD  Obesity hypoventilation syndrome (i.e., Pickwickian syndrome)  Neuromuscular disorders  Amyotrophic lateral sclerosis  Severe restrictive ventilatory defects  Interstitial fibrosis and  Thoracic deformities
  • 25. Respirator y Acidosis Symptoms:  Symptoms of the disease that causes respiratory acidosis are usually noticeable     shortness of breath easy fatigue chronic cough, or wheezing.  When respiratory acidosis becomes severe,    Confusion irritability, or lethargy may be apparent.
  • 26. Respirator y Acidosis Treatment:    Treat the underlying cause Improve alveolar gas exchange Assisted ventilation • Bicarbonate must not be infused to treat the acidosis because it generates more CO2
  • 27. Respiratory Alkalosis Hyperventilation,  PaCO 2 • • • • • • • • • • • Catastrophic CNS Events Hemorrhage Hysterical Assisted ventilation Drugs Salicylates (early stages) Interstitial Lung Disease Cirrhosis, Liver Failure Anxiety Gram negative Septicemia Hypoxia and severe anemia or high altitude
  • 28. Respiratory Alkalosis Symptoms • • • • • • Tingling and numbness Parasthesias Lethargy Tetany Unconsciousness Vasospasm of cerebral vassals Hypercapnia
  • 29. Respiratory Alkalosis Treatment • Treat underlying cause
  • 30. Metabolic Acidosis • Increased H+ Load • Increased HCO3- Loss
  • 31. Metabolic Acidosis
  • 32. Anion Gap Metabolic Acidosis Accumulation of unmeasured anions Low HCO3 and  AG AG AG HCO3Na+ HCO3Na+ Cl- Cl- • • • • • • • • M ethanol U remia D iabetic ketoacidosis P araldehyde I nfection L actic acid E thylene glycol S alicylates
  • 33. • • • • • • • Salicylates Lactic acidosis Uremia Methanol intoxication Paint sniffing (toluene) / Paraldehyde Ethylene glycol intoxication DKA or alcoholic ketoacidosis
  • 34. Non Anion Gap Metabolic Acidosis Loss of HCO3 or External acid infusion Low HCO3 AG < 12 • GI Losses of Bicarbonate (Diarrhoea) • Renal Losses • Renal Tubular Acidosis • Renal Toxins • Carbonic Anhydrase Inhibitors • Ureteral Diversion • Compensation for Resp. Acidosis • HCl or NH4Cl Infusion, TPN
  • 35. Decrease in Anion Gap Metabolic Acidosis Defined as < 6 P araproteinemias, Multiple myeloma L ithium intoxication E xcessive Calcium and Magnesium A lbumin is low (hypoalbuminemia) B romism
  • 36. Metabolic Acidosis Clinical Features • Increased work of breathing :  Deep rapid breathing (Kussmaul’s) • Peripheral Vasodilatation,  collapse, shock, impaired cardiac function • Lethargy, drowsiness, confusion, stupor • Hyperkalemia • Nonspecific : Nausea, Vomiting • Chronic Acidosis:  Osteopenia – CaCo loss 3  Muscle weakness – Glutamine loss
  • 37. Metabolic Acidosis Management Principles: • • Identify cause Initial goal : Bring the pH ~ 7.25 (For cardiac contractility & responsiveness to catecholamines) Sodabicarb : 1-2 mEq/Kg [1 ml of 7.5% NaHCO3 = 0.9 mEq] [Bicarb deficit (mEq/L) = Body wt.(Kg) X 0.3 X Base excess] • Half as bolus • Half as infusion over 12 – 24 hrs.
  • 38. Metabolic Acidosis Management – Contd. • Potassium replacement : Serum K+ should be > 3.5 mEq/L before administering HCO3 - • THAM (tromethamine; tris-hydroxymethyl aminomethane) An amino alcohol Indication : In partients with CHF who may not be able to tolerate additional Na+ burden if treated with Sodabicarb. Dose : Body wt. (Kg) X Base excess Administration: As infusion over 3 - 6 hours
  • 39. Metabolic Acidosis Specific Treatment • • • • • DKA Lactic Acidosis RTA Uremia Salicylate toxicity
  • 40. Metabolic Alkalosis Increase in extra-cellular pH (above 7.45) due to primary increase in plasma bicarbonate Very Dangerous: • Shifts O 2 dissociation curve to Lt. • Causes vasoconstriction of all vessels except pulmonary circulation • Suppresses ventilation • Decreases ionized Ca ++ and shifts K + into cells – hypocalcemia and hypokalemia
  • 41. Metabolic Alkalosis Issues to Ponder over: • What generated the alkalosis? • What is maintaining the alkalosis – what is preventing kidney from excreting the alkali ?
  • 42. Metabolic Alkalosis Causes • Loss of acid: GI Losses • • • Vomiting NG suction Acid diarrhoea (Congenital chloridorrhoeas, villous adenomas) Renal H+ Loss • Diuretics (thiazides, furosemide) • Bartter’s Syndrome • Mg deficiency • Hyperaldosteronism, Cushing’s • Infusion of HCO3: • Iatrogenic • Milk Alkali syndrome • Massive blood transfusion (citrated blood) • Rapid correction of chronic hypercapnia
  • 43. Metabolic Alkalosis What’s maintaining 1. Volume contraction (Chloride responsive) NG Suction, vomiting, diuretics 2. Potassium deficiency 3. Chloride depletion 4. Increased mineralocorticoids (Chloride resistant)
  • 44. •Metabolic Alkalosis What’s maintaining • • • • • • Volume contraction (Chloride responsive) Adrenal Disorders Exogenous Steroids Alkali Ingestion Licorice Bartter’s Syndrome
  • 45. •Metabolic Alkalosis Clinical Presentation • • • • Muscle cramps Weakness Hypoxia Arrhythmias
  • 46. •Metabolic Alkalosis Saline responsive    intravascular volume expansion with normal saline potassium repletion Ammonium chloride / Arginine chloride in resistant casessistant alkalosisgastric losses) Saline resistant     potassium repletion mineralocorticoid antagonists acetazolamide Hemo or peritoneal dialysis : in severe alkaloses with hyperosmolar states
  • 47. Mixed Acid – Base Disorders • Compensatory adjustments fall outside the expected reange • Respiratory Acidosis + Metabolic Acidosis – Resp. Distress Syndrome • Respiratory Acidosis + Metabolic Alkalosis – Excessive diuretic therapy, Chronic respiratory acidosis with C.C.F. • Metabolic Acidosis + Respiratory Acidosis – Hepatic Failure • Respiratory Alkalosis + Metabolic Acidosis – Salicylate intoxication – Gm – ve sepsis
  • 48. When to suspect a mixed acid base disorder: 1. The expected compensatory response does not occur 2. Compensatory response occurs, but level of compensation is inadequate or too extreme 3. Whenever the PCO2 and [HCO3-] becomes abnormal in the opposite direction. 4. pH is normal but PCO2 or HCO3- is abnormal 5. In anion gap metabolic acidosis, if the change in bicarbonate level is not proportional to the change of the anion gap. 6. In simple acid base disorders, the compensatory response should never return the pH to normal. If that happens, suspect a mixed disorder.
  • 49. • Vittal
  • 50. Case 1 : 5 mo. Old baby with bronchiolitis Measured Measured pH pH pCO2 pCO2 pO2 pO 370C 370C 7.24 7.24 60.0 mmHg 60.0 mmHg 56.0 mmHg 56.0 mmHg • Step 1: Calculated Calculated HCO3 actu HCO3 actu BE BE O2 Sat O Sat Data Data 24 mmol/L 24 mmol/L +2 +2 85% 85% • Step 3: Entered Data Entered Data FiO2 FiO 70 % 70 % 2 2 2 Alkalosis or Acidosis? • Step 2: Primary Disturbance? Acute or Chronic? pH - 0.08 X (60-40)/10 = 0.16 7.4-0.16 = 7.24
  • 51. Case 1: • • • • pH pCO2 HCO3BE Analysis: = 7.24 = 60 mm Hg = 24 mEq/L = +2 less than 7.35, so - acidosis CO2 is > 45 mm Hg.- Resp. is normal. is normal. Conclusion: Acute Resp.Acidosis – Uncompensated Note: A pH of 7.24 could not be caused by a bicarbonate value that is WNL.
  • 52. Case 2 : Measured Measured pH pH pCO2 pCO2 pO2 pO2 S.Na++ S.Na S.Cl - S.Cl Calculated Calculated HCO3- -actu HCO3 actu BE BE O2 Sat O2 Sat Entered Data Entered Data FiO2 FiO 2 3 yr. Old baby with severe diarrhoea, diminished urine output, lethargy 370C 370C 7.1 7.1 20.0 mmHg 20.0 mmHg 87.0 mmHg 87.0 mmHg 135 mEq 135 mEq 115 mEq 115 mEq Data Data 8 mmol/L 8 mmol/L -15 -15 96% 96% 24 % 24 % • Step 1: Alkalosis or Acidosis? • Step 2: Primary Disturbance? • Step 4: What is the Anion Gap? Na-(Cl+HCO3) 135-(115+8) = 12 • Step 6: What is the expected CO2? (1.5 X HCO3) + (8+2) = 1.5X 8) + (8+2) = 18-22 = 18-22 Metabolic Acidosis with Respiratory Compensation
  • 53. Case 3 : 8 mo.. Old baby resuscitated after a cardiac arrest; Na 142, Cl 108 Measured Measured pH pH pCO2 pCO2 pO2 pO 370C 370C 7.10 7.10 60.0 mmHg 60.0 mmHg 60.0 mmHg 60.0 mmHg • Step 1: Calculated Calculated HCO3 actu HCO3 actu BE BE O2 Sat O Sat Data Data 10 mmol/L 10 mmol/L -15 -15 87% 87% • Step 4: 2 2 Entered Data Entered Data FiO2 FiO 2 Alkalosis or Acidosis? • Step 2: Primary Disturbance? What is the Anion Gap? Na-(Cl+HCO3) 142-(108+10) = 24 • Step 5: 100 % 100 % What is the corrected HCO3? (Corrected HCO3 = HCO3 + (AG - 12) 10 + (24 - 12) = 22
  • 54. Case 3 : 8 mo.. Old baby resuscitated after a cardiac arrest; Na 142, Cl 108 Measured Measured pH pH pCO2 pCO2 pO2 pO 370C 370C 7.10 7.10 60.0 mmHg 60.0 mmHg 60.0 mmHg 60.0 mmHg • Step 6: Calculated Calculated HCO3 act HCO3 act BE BE O2 Sat O Sat Data Data 10 mmol/L 10 mmol/L -15 -15 87% 87% (1.5 X 10) + (8 + 2) = 21 – 25 2 2 Entered Data Entered Data FiO2 FiO 2 100 % 100 % What is the expected pCO2? (Expected pCO2 = (1.5 X HCO3 + (8+2) Mixed Metabolic & Respiratory Acidosis
  • 55. Case 4 : 4 yr. old girl with lethargy, irritability, jaundice Measured Measured pH pH pCO2 pCO2 pO2 pO 370C 370C 7.52 7.52 26.0 mmHg 26.0 mmHg 112.0 mmHg 112.0 mmHg Calculated Calculated HCO3 actu HCO3 actu BE BE O2 Sat O Sat Data Data 22 mmol/L 22 mmol/L +0.2 +0.2 99 % 99 % Entered Data Entered Data FiO2 FiO 33 % 33 % 2 2 2 • Step 1: Alkalosis or Acidosis? • Step 2: Primary Disturbance? • Step 3: Acute or Chronic? pH - 0.08 X (26-40)/10 = 0.12 7.4+0.12 = 7.52 Acute Respiratory Alkalosis – Uncompensated
  • 56. Exercises
  • 57. Exercise 1: pH = 7.2 PCO2 HCO3- = 60 mm Hg = 24 mEq/L SBE = 0 mEq/L Analysis: Overall change is acid. Respiratory change is also acid therefore contributing to the acidosis. Bicarb and SBE are normal - no metabolic compensation. Conclusion: Pure respiratory acidosis. Typical of acute respiratory depression. Magnitude: Marked respiratory acidosis
  • 58. Exercise 2: pH = 7.31 pCO2 = 44 mm Hg HCO3- = 20 mEq/L Analysis: pH is less than 7.35, so the condition is acidosis. pCO2 is normal. HCO3- is less than 24 mEq/L. Conclusion: This is an example of metabolic acidosis. Note: This is the same pH as the first example, but it is due to too little bicarbonate
  • 59. Exercise 3: pH = 7.48 pCO2 = 33 mm Hg HCO3- = 24 mEq/L Analysis: pH is more than 7.45, so the condition is alkalosis. pCO2 is below 35 mm Hg. HCO3- is normal. Conclusion: This is an example of respiratory alkalosis. Note: A pH of 7.48 could not be caused by a bicarbonate value that is WNL
  • 60. Exercise 4: pH = 7.48 pCO2 = 43 mm Hg HCO3- = 33 mEq/L Analysis: pH is more than 7.45, so the condition is alkalosis. pCO2 is normal. HCO3- is above 28mEq/L. Conclusion: This is an example of metabolic alkalosis. Note: This is the same pH as the third example, but it is due to too much bicarbonate.
  • 61. Exercise 5: pH = 7.4 pCO2 = 60 mm Hg HCO3- = 37 mEq/L Analysis: Note that the carbon dioxide and bicarbonate values are both abnormal, but The pH is WNL. In this case, the kidneys are retaining bicarbonate to counter the lungs’ retention of carbon dioxide, thus, keeping the 1 to 20 ratio and a pH that is WNL. Conclusion: respiratory acidosis with metabolic compensation
  • 62. Exercise 6: Analysis: pH = 7.18 CO2 = 41 mm Hg HCO3- = 14 mEq/L BE =-4 The respiratory value is WNL, Bicarbonate is below normal. Base excess is actually a deficit (-4). There is a true deficit of bicarbonate. e.g. diabetic ketoacidosis. Conclusion: Metabolic acidosis where, as yet, there is no compensation by the lungs.