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ACID-BASE BALANCE

ACID-BASE BALANCE. ACID-BASE BALANCE. Dr. Özge Köner Y.T.U. Hospital Anesthesiology Dept. Dr. Özge Köner YTÜ Hastanesi Anesteziyoloji A.D. Acid base imbalance:.

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ACID-BASE BALANCE

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  1. ACID-BASE BALANCE ACID-BASE BALANCE Dr. Özge Köner Y.T.U. Hospital Anesthesiology Dept. Dr. Özge Köner YTÜ Hastanesi Anesteziyoloji A.D

  2. Acid base imbalance: • Severe acid-base imbalance may lead to organ failure, such as brain edema, seizure activity, myocardial dysfunction and pulmonary vasoconstriction, systemic vasodilation. • Immune cell dysfunction

  3. Acid-Base balance is determined by the electric neutrality of the aqueous fluidsTotal Cation = Total AnionAcidity of the body fluids is determined by the free H+ concentration.H2O H+ + OH-

  4. Acid: donates H+ ion Base: takes up H+ ion Acidemia: pHa <7,35 Acidosis: pathology leading to arterial pH Alkalemia: pHa >7,45 Alkalosis: arterial pH

  5. Chemistry pH =7 neutral Blood pH7.4 neutral [ H+] = 40 nM blood pH < 6,8 & > 7,8 FATAL !

  6. pH: - log[H+]Henderson-Hasselbalch equationpH=pKa + HCO3-/CO2pH is correlated with the ratio of dissociate anion to non-dissociate acid. 1909 & 1916 The effects of nonbicarbonate tampons & serum electrolytes ??

  7. Independent factors determining ACID-BASE balance Steward approach (1983) • SID (strong ion difference) (strong cations-strong anions)=(40-42 mEq/L) (Na+K+Ca+Mg) – (Cl+organic anions -lactate, keton bodies-) • PaCO2 • Total nonvolatile weak acids (Atot) (albumine, phosphate) H+, OH- & HCO3- is changed secondarily in response to changes of the aforementioned independent factors.

  8. SID = 40-42 mEq/L (Na +K+Ca+Mg) – (Cl+organic anions) • If Na : SID, pHa is increased: (ALKALOSIS) Increased SID decreases dissosiation of water (H2O H++OH-) • If Cl : SID, pHa is decreased: (ACIDOSIS) Decreased SID decreases dissosiation of water. (H2O H++OH-)

  9. Acid-Base Disturbances

  10. ΔHCO3: 1 mEq/L for every 10 mmHg CO2 increase Acute Resp Acidosis ΔHCO3: 2 mEq/L for every 10 mmHg CO2 decrease AcuteRespAlkalosis ChronicRespAcidosis ΔHCO3: 4-5 mEq/L for every 10 mmHg CO2 increase ΔHCO3: 4-5 mEq/L for every 10 mmHg CO2 decrease ChronicRespAlkalosis paCO2: 1.5 x HCO3 + 8 ± 2 MetabolicAcidosis paCO2: 0.7 x (HCO3- 24) + 40 ± 2 MetabolicAlkalosis

  11. COMPANSATORY MECHANISMS • Acute Chemical Compansation • Respiratory Compansation • Renal Compansation

  12. 1-Chemical tampon system • HCO3-/H2CO3* -extracellular-fast 15-20 mins • Hb (HbH/Hb-) -extracellular, tampons volatile+nonvolatile acids • Proteins (PrH/Pr-) –intracellular-slow 2-4 hrs • HPO4/H2PO4 –urinary, intracellular • NH3/NH4+ -urinary

  13. 2-Pulmonary Compansation Chemoreceptors sensitive to the pH within the CSF leads to increased or decreased CO2 levels. 1 mmHg increment of CO2 may increase minute ventilation by 1-4 L. FAST COMPANSATION

  14. Pulmonary Compansation in Metabolic Acidosis • Alveolar hyperventilation (pCO2 ) • pH can not reach the physiologic limit • Stabilized within 12-24 hrs.

  15. Pulmonary Compansation inMetabolic Alkalosis Increased pH Respiratory center depression Hypoxemia PaCO2 increased (>55mmHg) pH becomes physiologic Respcenterstimulation Compansation is limited Stabilized within 24-36 hours

  16. 3- Renal Compansation

  17. Alkalosis Acidosis

  18. Renal Compansation in Acidosis: SLOW, begins within 6-12 hrs, peaks at 2-5 days. • Reabsorbtion of the filtered HCO3- • Titrable acid elimination (H2PO4) H+ elimination • Ammonium elimination (NH4+) Tubular H+ secretion & HCO3 reabsorbtion

  19. Renal Compansation in Alkalosis (very effective) • Compansation: large amount of HCO3 elimination. • However, Na deficit or Excess Mineralocorticoid levels may lead to Metabolic Alkalosis

  20. Renal Compansation insufficiency in Alkalosis • Na deficiency (ECF decreased): At proximal tubul Na+, Cl-,HCO3- reabsorbtion is increased, H+ is secreted. • If Mineralocorticoid activity is increased: Na+ reabsorbed & H+ secreted from distal tubulus (Aldosteron). The result is increased HCO3 & augmented metabolic alkalosis.

  21. METABOLIC ACIDOSIS Decreased SID, increased Atot & H+ Anion Gap Acidosis: AG=(Na+K)–(Cl+HCO3): 3-12 mEq/L • Lactic acidosis accounts for about half the cases. It is often due to shock or tissue hypoxia. • Renal: RTA-1,2,4 • GİS losses: Diarrhea, fistulas B. INCREASED Chloride level • Dilutional: large amount of HCO3 free fluids (%09 NaCl infusion) • Acetazolamide • Bladder reconstruction • Mineralocorticoid deficiency • Increased intake of Cl- containing acids • Ammonium chloride, lysine HCl, Arginine HCl, TPN solution Normal anion Gap Acidosis: A. HCO3 loss

  22. Metabolic alkalosis & hypoalbuminemia • Albumin (weak acid) is not taken into account during Anion Gap calculation. However, it may account for up to 75% of the anion gap. • For every decrement of 1 g/dL in the serum albumin, the calculated Anion Gap should be increased by approximately 2,3 to 2,5 mmol/L.

  23. ANION GAP METABOLIC ACIDOSIS (MUDPILES) Methanol Uremia Diabeticketoacidosis Propylene-ethylene glycole (solvent) Infection, isoniazid, iron Lactic acidosis Etilen glycol, Ethanol Salicylate Rhabdomyolysis

  24. NORMAL ANION GAP METABOLIC ACIDOSIS (FUSEDCARS) Fistula (pancreatic) Ureteroenterostomy Saline infusion Endocrine (hyperparathyroidism) Diarrhea Carbonic anhydrase inhibitors Amonyum chloride Renal tubular acidosis Spiranolactone

  25. METABOLIC ACIDOSIS THERAPY Treatment of theunderlyingfactors Respiratorycompansation If it is chronic SID should be corrected. (Na+ replacement) IfpH < 7.10, NaHCO3 ?? Deep, refractoryacidosis: Hemodialysis

  26. METABOLIC ACIDOSIS TREATMENT NaHCO3 disadvantages: Hypertonisity Intracellular acidosis (due to increased paCO2).

  27. METABOLIC ALKALOSISIncreased SID, decreased Atot, hypovolemia • Cl sensitive– UCL<25 mmol/LGIS losses (Cl loss) NaCl loss, ECF deficit Diuretic (contraction alkalosis) Cystic fibrosis • Cl resistant UCL>40: Mineralocorticoid excess (Na retention, renal H loss) Severe hypokalemia (H diffuses into the cell) Bartter synd, Gitelman syndrome Extreme hypercalcemia, severe hypomagnesemia • Various: Massive blood transfusion (citrate), Lactate, Acetate solution, Na-penicillin, NaHCO3, hypercalcemia, alkali treatment in renal insufficiency.

  28. METABOLIC ALKALOSIS TREATMENT • Cl sensitive: CL replacement NaCl (large amount), KCl, HCl • Cl resistant: Aldosteron antagonist Acetazolamide (edematous patients): 5-10 mg/kg oral • pH>7,60: iv HCL (0,1 N) or Hemodialysis In Metabolic Alkalosis, SID is increased due to : Cl loss or increased Na.

  29. RESPIRATORY ACIDOSIS • CNS depression CNS diseases, drugs, sleep-apnea, obesity, • Neuromusculary disorders M.gravis, G.barre, myopathies, hipopotasemia • LUNG disease/Pleural abnormalities Asthma, ARDS, COPD, lung edema-fibrosis, pneumonia, pneumothorax • Chest wall abnormalities (cot fracture, flail chest) • Upper airway obstruction (croup, foreign body) • Mechanical hypoventilation • Increased CO2 production: m.hyperthermia, intensive shivering, large caloric intake, prolonged seizure activity, thyroid storm, extensive thermal injury

  30. Respiratory Acidosis Tissue CO2 production is more than its elimination. • Acute CO2 increase: blood H+ and HCO3- Compansation: • SID is increased • Increased H+ is decreased back to normal. • Cl- is eliminated via renal route.

  31. Respiratory AcidosisTreatment • Mechanical ventilation • Nutritional carbonhydrate content should be decreased • Fever control • Shivering control

  32. RESPIRATORY ALKALOSIS • CNS stimulation: Pain, anxiety, stroke, ischemia, tumor, infection, fever, drugs (salisilat, progesterone-pregnancy-, teophyillin, chatecolamine, analeptics-doxapram), liverdysfunction. • Peripheralstimulation: • Hypoxemia • High altitude • Pulmonarydisease (CHF, Noncardiogenic PE, Asthma, P.Embolism) • Severe anemia • Unknownmechanism: Sepsis, Metabolicencephalopathy • Iatrogenic: Ventilator-induced

  33. pH pH <7.35 pH >7.45 HCO3 <22 paCO2 >40 paCO2 <40 HCO3 >26 METABOLIC ACIDOSIS RESPIRATORY ACIDOSIS RESPIRATORY ALKALOSIS METABOLIC ALKALOSIS CALCULATE ANION GAP URINARY Cl- ACIDOSIS ALKALOSIS If HCO3 & CO2 does’t change in the same direction for compansation or the compansation is beyond the expected value, “mixed type” acid-base disturbance is likely.

  34. COMPANSATORY RESPONSE • RESPIRATORY: • Acute resp alkalosis: HCO3 should be decreased by 2 mmol/L for every 10 mmHg paCO2 decrease below 40. • Acute resp acidosis: HCO3 should be increased by 1 mmol/L for every 10 mmHg paCO2 increase. • If the event is chronic the change is 4-5 mmol/l. • METABOLIC: • Alkalosis: Expected pCO2=0.7 x (HCO3- 24) + 40 ± 2 • Acidosis:ExpectedpCO2: 1.5 x HCO3 + 8 ± 2 • If the compansation is beyond those or HCO3 & CO2 is in opposite directions then mixed type acid-base disorder is likely.

  35. 1. ALKALOSIS NO a. EXCESS HCO3 ? b. INCREASED CO2 elimination ? YES RESPIRATORY ALKALOSIS ; Renal compansation by means of HCO3elimination.

  36. 1. ACIDOSIS a. ACIDOSISdue to CO2 retension ? NO b. ACIDOSIS due to increased HCO3 elimination ? YES Metabolic Acidosis:Respiratory Compansation

  37. 1/12 M. Ao stenosis, annuloplasty postop. CHF: tachypnea, oliguria, Hepatomegaly, Cardiomegali. Intubation-Mechanical Ventilation, Spontaneous breaths (FiO2: 1) • pH: 7,49 • pCO2: 15 mmHg • paO2: 200 mmHg • HCO3: 7,7 mEq/L • BE: -14,6 • Hb: 9,5 • Na: 135 • Cl: 95 • K: 5,5 pH > 7,45 pCO2 < 40 expected HCO3 fall: Acute respiratory alkalosis (for every 10mmHg, 2 mEq/L change): 5 mEq/L Lactate:14,4 mEq/L (Normal value <2.5)

  38. Respiratory Alkalosis+Metabolic Acidosis- Mixed Type ANION GAP: (135+5.5) -(95+8) = 36.5 mEq/L (Lactate: 14.4 mEq/L) LACTIC ACIDOSIS + hyperventilation due to CHF, pain, infection ??

  39. TREATMENT • CHF treatment (digitalis, furosemide) • Raise the Hb level (12-14 g/L): RBC transfusion.

  40. 24 hrs after the treatment, tachypnea is decreased, blood pressure is 100/50 mmHg, FiO2 0.5. pH: 7,51 pCO2: 40 mmHg paO2: 124 mmHg HCO3: 28 mEq/L BE: 5 Hb: 14 Na: 136 Cl: 91 Urinary Cl=10 K: 3.2 Lactate 2.7 mmol/L

  41. Metabolic Alkalosis Due to loop DIURETIC. TREATMENT: IV KCL infusion Saline infusion (small volume) NaCL

  42. 45 y/o male, traffic accident; intraabdominal bleeding. Blood pressure 90/50 mmHg, HR 120/dk, RR 36/dk temp:35 oC pH: 7.28 pH < 7.35 pCO2: 24 mmHgpCO2 < 35 pO2: 80 mmHg HCO3: 10 mEq/L Albumine: 4 g/dL BE: -16 (<-5) Lactate: 16 mmol/L Na: 144 mmol/L A.Gap= 26 K: 4 mmol/L Cl: 110 mmol/L Ure: 10 Creatinine: 2 g/dL

  43. METABOLIC ACIDOSISRespiratory compensation Expected pCO2 = 23 mmHg pCO2 = 1,5 x HCO3 (+8)±2 = 1,5 x 10 (+8) = 23

  44. 45 y/o F Prolonged vomitingExamination: Skin turgor is decreased, CVP is low, BP= 100/60 mmHg pH: 7.53 pCO2: 48 mmHg pO2: 90 mmHg Sat: 98% HCO3: 42 mEq/L Urinary pH: 5 Na: 140 mEq/L UNa: 2 Cl: 86 mEq/L UCl: 3 K: 2.2 UK: 21

  45. Hypochloremic METABOLIC ALKALOSIS Expected pCO2 = 44-48 mmHg ΔpaCO2 = [(0.7 x HCO3) – 24] +40 ± 2 (30 – 24) + 40 ± 2 = 48 RESPIRATORY COMPANSATION

  46. 4 y/o, F Severe diarrhea Exam: Skin turgor is decreased, BP is low, HR: 135, CVP=0 pH: 7.02 pCO2: 13 mmHg HCO3: 3 mEq/L pO2: 70 mmHg Sat: 96% Na: 130 mEq/L Cl: 106 mEq/L K: 3

  47. METABOLIC ACIDOSIS Expected pCO2 = 12.5 mmHg pCO2 = 1.5 x HCO3 +8= 12.5 ± 2 RESPIRATORY COMPANSATION

  48. 42 y/o male, IDDM, PONV for 2 days, stops insulin due to the insufficient oral intake. pH: 7,21 pCO2 25 HCO3 10 Na 133 mEq/l Cl 88 mEq/l K 5 mEq/l ACIDOSIS METABOLIC ANION GAP ? = 35 DIABETIC KETOACIDOSIS Respiratory alkalosis (Compansation) Expected pCO2: 1.5 x HCO3+8 ± 2 = 21-25 mmHg

  49. 70 y/o male, IDDM, chronic renal disease (creat 2.0); ischemic heart disease, EF %25-30; 8 kg weight gain within the last week, pretibial edema, crepitation with lung oscultation; mask O2 -0.6 FiO2. BP: 130/65; HR: 90/min. pH : 7.17 pH < 7,40 pCO2 : 60 mmHg pCO2 > 40 HCO3: 18 mEq/L BE : -7.5 paO2 : 83 mmHg Sat : 94% Na : 148 mEq/L Cl : 110 mEq/L K: 4.7 Hb: 10 g/dL Blood glucose: 180 g/dL

  50. 50 y/o male, postoperative multiorgan failure: Measured values: Calculated values: pH : 7.40 HCO3 : 24 pCO2 : 39 mmHg Clcorr : 106 mEq/L BE lab: 0 ΔAGcorr: 13 mEq/L Mg : 1.6 mEq/L SIG: 19 mEq/L (ref.0) Ca : 3.4 mEq/L Na : 137 mEq/L Cl : 102 mEq/L K : 4.9 Albumine: 6 g/L (35-55 g/dL) Pi : 0.3 mmol/L (1-1.5)

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