Acid base imbalance in medicine

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  • Acid base imbalance in medicine

    1. 1. Acid- Base Balance Dr. Omar Mohamed DanfourSenior Lecturer –Specialist of Anesthesia & Intensive Care 1 (MSU-IMS-Anesthesia Department
    2. 2. pH Review• PH = - log [H+]• H+ is really a proton• If [H+] is high, the solution is acidic  pH• If [H+] is low, the solution is basic or alkaline pH• Acids are H+ donors.• Bases are H+ acceptors, or give up OH- in solution.• Acids and bases can be: – Strong – dissociate completely in solution • HCl, NaOH – Weak – dissociate only partially in solution • Lactic acid, carbonic acid 2
    3. 3. Acid Base -Basic Concepts• Hydrogen Ion [H+] is tightly controlled• [H+] is determined by the balance between PaCO2 and serum HCO3 (bicarbonate), {normal ratio is 20 (Hco3) : 1(H2Co3)} Henderson-Hasselbalch Equation [H+] = 24 (PaCO2 / HCO3-) Normal Values – [H+] = 40 nEq/L – pH = 7.40 (7.35-7.45) – PaCO2 = 40 mm Hg (35-45) – HCO3 = 24 mEq/L (22-26) – < 6.8 or > 8.0 death occurs 3
    4. 4. [H+] pH pH = 6.1 + log ([PaCO2] / [0.03 x HCO3-])pH [H+] pH [H+]7.80 16 7.30 507.75 18 7.25 567.70 20 7.20 637.65 22 7.15 717.60 25 7.10 797.55 28 7.00 897.50 32 6.95 1007.45 35 6.90 1127.40 40 6.85 1417.35 45 6.80 159 4
    5. 5. Keep It Simple• PaCO2 = Acid –  PaCO2 =  pH (Acidemia) –  PaCO2 =  pH (Alkalemia)• HCO3 = Base –  HCO3 =  pH (Alkalemia) –  HCO3 =  pH (Acidemia)• Acidosis: pH < 7.35 – Respiratory PaCO > 40 mmHg – Metabolic HCO3 < 24 mEq/L• Alkalosis: pH > 7.45 – Respiratory PaCO2 < 40 mmHg 5
    6. 6. The Body and pH 6
    7. 7. Simple Acid-Base Disorders Type of Disorder pH PaCO2 [HCO3]Metabolic Acidosis ↓ ↓ ↓Metabolic Alkalosis ↑ ↑ ↑Acute Respiratory Acidosis ↓ ↑ ↑Chronic Respiratory Acidosis ↓ ↑ ↑↑Acute Respiratory Alkalosis ↑ ↓ ↓Chronic Respiratory Alkalosis ↑ ↓ ↓↓ 7
    8. 8. Small changes in pH can produce major disturbances• Most enzymes function only with narrow pH ranges• Acid-base balance can also affect electrolytes (Na+, K+, Ca++, Cl-)• Can also affect hormones• The body produces more acids than bases• Acids take in with foods• Acids produced by metabolism of lipids and proteins• Cellular metabolism produces CO2.• CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3- 8
    9. 9. Control of Acids 1. Buffer systems  Take up H+ or release H+ as conditions change  Buffer pairs – weak acid and a base  Exchange a strong acid or base for a weak one  Results in a much smaller pH change CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3- Bicarbonate buffer• Sodium Bicarbonate (NaHCO3) and carbonic acid (H2CO3)• Maintain a 20:1 ratio : HCO3- : H2CO3 HCl strong Acid + NaHCO3 weak Base ↔ H2CO3 weak acid + NaCl 9
    10. 10. Phosphate buffer• Major intracellular buffer• H+(acid) + HPO42- ↔ H2PO4- (titratable acids eliminated in urine)• OH-(Base) + H2PO4-acid ↔ H2O + H2PO42- Protein Buffers• Hemoglobin is rich in histidine which is an effective buffer from PH5.7 to 7.7.(Hb in RBCs in equilibrium as a weak acid(HHB) and a potassium salt (KHb)• Carboxyl group gives up H+• Amino Group accepts H+• Side chains that can buffer H+ are present on 27 10
    11. 11. 2. Respiratory mechanisms• Exhalation of carbon dioxide• Powerful, but only works with volatile acids• Doesn’t affect fixed acids like lactic acid• CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3-• Body pH can be adjusted by changing rate and depth of breathing 3. Kidney excretion• Can eliminate large amounts of acid• Can also excrete base• Can conserve and produce bicarb ions• Most effective regulator of pH• If kidneys fail, pH balance fails 11
    12. 12. Rates of correction• Buffers function almost instantaneously (rapid)• Respiratory mechanisms take several minutes to hours• Renal mechanisms may take several hours to days 12
    13. 13. 13
    14. 14. Acid-Base Imbalances• pH< 7.35 acidosis• pH > 7.45 alkalosis• The body response to acid-base imbalance is called compensation• May be complete if brought back within normal limits• Partial compensation if range is still outside normals• If underlying problem is metabolic, hyperventilation or hypoventilation can help : respiratory compensation.• If problem is respiratory, renal mechanisms can bring about metabolic compensation 14
    15. 15. 15
    16. 16. Respiratory Acidosis• Carbonic acid excess caused by blood levels of CO2 above 45 mm Hg.• Hypercapnia – high levels of CO2 in bloodCauses:• Chronic conditions: – Depression of respiratory center in brain that controls breathing rate – drugs or head trauma – Paralysis of respiratory or chest muscles – COPD, pneumonia & obesity CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3- 16
    17. 17. Respiratory Acidosis• Acute conditons: – Adult Respiratory Distress Syndrome – Pulmonary edema – Pneumothorax – Pulmonary emboli – Aspiration pneumonia – Increased CO2 production (Malignant hyperthermia & thyroid storm) 17
    18. 18. Signs and Symptoms of Respiratory Acidosis• Breathlessness• Restlessness• Lethargy and disorientation• Tremors, convulsions, coma• Respiratory rate rapid, then gradually depressed• Skin warm and flushed due to vasodilation caused by excess CO2 18
    19. 19. Compensation for Respiratory Acidosis• This is accomplished via two mechanisms; a) rapid cell buffering and• In this setting, carbonic acid (H2CO3 ) can only be buffered by the limited intracellular buffers (primarily hemoglobin and proteins). H2CO3 + Hb- → HHb + HCO3- b) an increase in net acid excretion.• Kidneys eliminate hydrogen ion and retain bicarbonate ion (Chronic state) 19
    20. 20. 20
    21. 21. Treatment of Respiratory Acidosis• Restore & improve alveolar ventilation• IV lactate solution (converted to bicarbonate ions in the liver).• Treat underlying dysfunction or disease e.g. pul odema, Res depression 21
    22. 22. Respiratory Alkalosis• Carbonic acid deficit• pCO2 less than 35 mm Hg (hypocapnea)• Most common acid-base imbalance• Primary cause is hyperventilation CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3- 22
    23. 23. Respiratory Alkalosis• Conditions that stimulate respiratory center: – Oxygen deficiency at high altitudes – Pulmonary disease and Congestive heart failure – caused by hypoxia – Acute anxiety & pain – Fever, anemia – Early salicylate intoxication – Cirrhosis – Gram-negative sepsis – Iatrogenic (ventilator induced) 23
    24. 24. Signs and Symptoms of Respiratory Alkalosis • Alkalosis causes over excitability of the central and peripheral nervous systems. • Numbness • Light headedness • It can cause : – Nervousness – muscle spasms or tetany – Convulsions – Loss of consciousness – Death 24
    25. 25. Compensation of Respiratory Alkalosis• There are two mechanisms responsible for this compensation to respiratory alkalosis;1) Rapid cell buffering and2) Decrease in net renal acid excretion.• hydrogen ions move from the cells into the extracellular fluid, where they combine with [HCO3- to form carbonic acid in the following reaction: H+ + HCO3- → H2CO3 (CA)• In acute respiratory alkalosis, for every 10 mmHg decrease in the PCO2, there is a 2meq/L decrease in the plasma HCO3- concentration.• In chronic state renal compensation result in a 4 meq/L reduction in plasma [HCO3-] for every 10 mmHg reduction in PCO2. 25
    26. 26. 26
    27. 27. Treatment of Respiratory Alkalosis• Treat underlying cause• Breathe into a paper bag ???• IV Chloride containing solution (hydrochloric acid, arginine chloride & ammonium chloride), Cl- ions replace lost bicarbonate ions 27
    28. 28. Metabolic Acidosis• Bicarbonate deficit - blood concentrations of bicarb drop below 22mEq/L• Occurs when pH falls below 7.35• Causes: – Loss of bicarbonate through diarrhea or renal dysfunction – Accumulation of acids (lactic acid or ketones) – Failure of kidneys to excrete H+ [H+] = 24 ×(PCO2 / [HCO3-]) CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3- 28
    29. 29. Two types of Metabolic Acidosis – High Anion Gap = net gain of acid – Normal anion gap = loss of bicarbonate Anion Gap Calculation• [Na+ + K+] – [Cl + HCO3] (Normal = 12 + 2) E.g :- Na 140, k 4 , CL 114, HCO3 18 (140 + 4) – (114 + 18) 144 – 132 = 12 normalE.g:- Na 140 , Cl 104, K 4.0, HCO3 10 (144) – (114) = 30 = High anion gap 29
    30. 30. Normal Anion Gap High Anion Gap Differential (USED CARP) (MUDPILES)• Ureterostomy • Methanol• Small bowel fistula • Uremia• Extra Chloride • DKA• Diarrhea • Paraldehyde• Carbonic anhydrase • Inborn inhibitors Errors• Addison’s disease • Lactic• Renal tubular acidosis Acidosis• Pancreatic fistulas • Ethylene Glycol Treatment: Replace • Salicylates 30
    31. 31. Symptoms of Metabolic Acidosis• Headache, lethargy• Nausea, vomiting, diarrhea• Coma• Death Compensation for Metabolic Acidosis• Increased ventilation• Renal excretion of hydrogen ions if possible• K+ exchanges with excess H+ in ECF( H+ into cells, K+ out of cells) CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3- 31
    32. 32. Compensation• Respiratory compensation results in a 1.2 mmHg reduction in PCO2 for every 1.0 meq/L reduction in the plasma HCO3- concentration down to a minimum PCO2 of 10 to 15mmHg.For example, if an acid load lowers the plasma HCO3-concentration to 9 meq/L, then:Degree of HCO3- reduction is 24 (optimal value) – 9 =15.Therefore, PCO2 reduction should be 15 × 1.2 = 18.Then PCO2 measured should be 40 (optimal value) – 18= 22mmHg. 32
    33. 33. 33
    34. 34. Treatment of Metabolic Acidosis• Treat the causes• Improve renal perfusion & acid excretion• NaHCO3, Dose = (weight Kg x base deficit x 0.3)• Ensure adequate ventilation 34
    35. 35. Metabolic Alkalosis• Characterized by – Primary ↑ in HCO3 concentration greater than 26 mEq/ L – Compensatory ↑ in PaCO2• Classified according to urinary chloride – Chloride responsive – Chloride resistant 35
    36. 36. Metabolic Alkalosis Chloride Responsive Urine Cl- < 20 mEq/LCauses• Volume Contraction: – Nasogastric suctioning, Gastric fistula – Vomiting , pyloric stenosis• Post Hypercapnia• Low chloride intake• Hypomagnesemia• Penicillin • Cystic fibrosis (sweat) • Alkali therapy (NaHCO3, Antacid abuse) • Chloride depletion (Diarrhoea & Diuretics 36
    37. 37. Metabolic Alkalosis Chloride Unresponsive (resistant) Urine Cl- > 20 mEq/L• Mineralcorticoid excess e.g Hyperaldosteronism• Exogenous steroids, Cushing’s disease• Alkali Ingestion• Licorice ingestion• Too much wine• Tobacco chewers• Bartter’s Syndrome 37
    38. 38. Symptoms of Metabolic Alkalosis• Respiration slow and shallow• Hyperactive reflexes ; tetany• Often related to depletion of electrolytes• Dysrhythmias Compensation for Metabolic Alkalosis• Alkalosis most commonly occurs with renal dysfunction, so can’t count on kidneys• Alkali load• Acid loss - vomiting• Respiratory compensation difficult (hypoventilation limited by hypoxia) 38
    39. 39. Compensation contn.• The development of alkalemia is sensed by central and peripheral chemoreceptors, resulting in a reduction in the rate of ventilation and a reduction in tidal volume and thus an elevation in the pCO2.pCO2 rises 0.7 mmHg for every 1.0 meq/L increment in theplasma [HCO3-].For example, if an alkali load raises the the plasma HCO3-concentration to 34 meq/L, then:Degree of HCO3- elevation is 34 – 24 (optimal value)= 10.Therefore, PCO2 elevation should be 0.7 × 10 = 7Then PCO2 measured should be 40 (optimal value) +7 =47mmHg. 39
    40. 40. 40
    41. 41. Treatment of Metabolic Alkalosis• Electrolytes to replace those lost• Treat underlying disorder• IV chloride containing solution e.g saline (Chloride Responsive)• Aldosterone antagonist (Chloride resistant) 41
    42. 42. Miscellaneous 1Arterial pH is related to the ratio of PCO2 to HCO3, both pulmonary & renal compensatory mechanism are always such that PCO2 and HCO3 change in the same direction.the exception occurs when there is a mixed acid base disorder. In that situation, multiple acid base processes coexisting may lead to a normal pH or a mixed picture especially when PCO2 & HCO3 moves in opposite directionIf the compensatory response is more or less than expected, by definition a mixed acid-base disorder 42 exist.
    43. 43. An Alternative ApproachAn Alternative Approach that is rapid but perhaps less precise is to correlate changes in Ph with changes in CO2 or HCO3.• For a respiratory disturbance, every 10mmHg changes in CO2 should change arterial PH by approximately 0.08 U in the opposite direction.• During metabolic disturbance, every 6mEq change in HCO3 also changes arterial PH by 0,1 in the same direction.• If the change in pH exceed or is less than predicted, a mixed acid-base disorder is likely to be present.• If the Arterial pH is relatively normal and the PCO2 and/or HCO3 are abnormal, one can assume that a mixed 43
    44. 44. Miscellaneous 2 • The Delta Ratio (∆/∆) • Assessment of elevated anion gap metabolic acidosis to determine if a mixed acid base disorder is present.Delta ratio = ∆ Anion gap/∆ [HCO3-] or ↑anion gap/ ↓ [HCO3-] = Measured anion gap – Normal anion gap Normal [HCO3-] – Measured [HCO3-] = (AG – 12) (24 - [HCO3-]) 44
    45. 45. Miscellaneous contDelta ratio Assessment Guidelines < 0.4 Hyperchloremic normal anion gap acidosis <1 High AG & normal AG acidosis 1 to 2 Pure Anion Gap Acidosis Lactic acidosis: average value 1.6 DKA more likely to have a ratio closer to 1 due to urine ketone loss High AG acidosis and a concurrent metabolic alkalosis >2 or a pre-existing compensated respiratory acidosis45
    46. 46. Compensation Primary Disorder Compensatory Mechanism Metabolic acidosis Increased ventilationMetabolic alkalosis Decreased ventilationRespiratory acidosis Increased renal reabsorption of HCO3- in the proximal tubule Increased renal excretion of H in the distal tubuleRespiratory alkalosis Decreased renal reabsorption of HCO3- in the proximal tubule Decreased renal excretion of H+ in the 46
    47. 47. Compensator Compensatory Initial Expected levelPrimary y chemicaldisorder change compensation Mechanism response PCO2 = (1.5 × [HCO3-]) + ± 2Metabolic ↓HCO3- ↓PCO2 Hyperventilation ↓PCO2 = 1.2 ×∆ [HCO3-]Acidosis PCO2 = (0.9 × [HCO3-]) +Metabolic 16 ± 2 ↑HCO3- ↑PCO2 HypoventilationAlkalosis ↑PCO2 = 0.7 × ∆ [HCO3-]Respiratory ↑PCO2 ↑HCO3-    Acidosis Intracellular Buffering ↑[HCO3-] = 1 mEq/L forAcute     (hemoglobin, every 10 mm Hg ∆PCO2 intracellular proteins) Generation of new HCO3- due to the ↑[HCO3-] = 3.5 mEq/L forChronic     increased excretion every 10 mm Hg ∆PCO2 of ammonium.Respiratory ↓PCO2 ↓HCO3-    Alkalosis Intracellular ↓[HCO3-] = 2 mEq/L forAcute     Buffering every 10 mm Hg ∆PCO2 Decreased reabsorption of 47 ↓[HCO3-] =4 mEq/L for
    48. 48. Acidemia (PH<7.35) PCO2 Normal High Or low Incompatible Normal [HCO3] [HCO3] or high Low Low High Normal MixedChronic Acute respiratoryrespiratory respiratory and metabolic Metabolicacidosis acidosis acidosis acidosis 48
    49. 49. ↓ Plasma [HCO3] Anion gap Normal Increased High anion gap Plasma [K] metabolic acidosis Low Normal High Respiratory HyperkalemicHypokalemic alkalosishyperchloremic hyperchloremicmetabolic acidosis metabolic acidosis 49
    50. 50. Alkalemia (PH>7.45) PCO2 Low HighNormal Normal[HCO3] Incompatible or [HCO3] Low High High Low NormalMixed Acute Chronic Metabolicrespiratory and respiratory respiratory alkalosismetabolicalkalosis alkalosis alkalosis 50
    51. 51. ↑ Plasma [HCO3]Metabolic alkalosis Respiratory acidosisSpot urine [Cl] >20mmolL <20mmolL Saline Saline responsive unresponsive metabolic alkalosis metabolic alkalosis 51
    52. 52. Example• A patient is in intensive care because he suffered a severe myocardial infarction 3 days ago. The lab reports the following values from an arterial blood sample: – pH 7.3 – HCO3- = 20 mEq / L ( 22 - 26) – pCO2 = 32 mm Hg (35 - 45) Diagnosis• Metabolic acidosis• With partial compensation 52
    53. 53. CASE 1• A 44 year old moderately dehydrated man was admitted with a two day history of acute severe diarrhea. Electrolyte results: Na+ 134, K+ 2.9, Cl- 108, HCO3- 16,• Urea 31, Cr 1.5.• ABG: pH 7.31 pCO2 33 mmHg HCO3 16 pO2 93 mmHg 53
    54. 54. CASE 2• A 22 year old female with type I DM, presents to the emergency department with a 1 day history of nausea, vomiting, polyuria, polydypsia and vague abdominal pain. P.E. noted for deep sighing breathing, orthostatic hypotension, and dry mucous membranes.• Labs: Na 132 , K 6.0, Cl 93, HCO3- 11 glucose 720, Urea 38, Cr 2.6. UA: pH 5, SG 1.010, ketones negative, glucose positive . Plasma ketones trace. ABG: pH 7.27 HCO3- 10 PCO2 23• What is the acid base disorder? 54
    55. 55. CASE 3• A 70 year old man with history of CHF presents with increased shortness of breath and leg swelling. ABG: pH 7.24, PCO2 60 mmHg, PO2 52 HCO3- 27• What is the acid base disorder? 55

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