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بسم الله الرحمن الرحيم

بسم الله الرحمن الرحيم. ABG Dr.Jarahzadeh Intensivist. Introduction. Acids and Alkali are produced continuously in body. Daily Production of acid: 1.Carbonic Acid : 15000 meq/day -From the metabolism of carbohydrates and fat -Excreted by lungs

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بسم الله الرحمن الرحيم

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  1. بسم الله الرحمن الرحيم

  2. ABGDr.JarahzadehIntensivist

  3. Introduction • Acids and Alkali are produced continuously in body. • Daily Production of acid: 1.Carbonic Acid : 15000 meq/day -From the metabolism of carbohydrates and fat -Excreted by lungs 2.Non-carbonic acids (Organic):50-100 meq/day -From the metabolism of proteins -Excreted by kidneys

  4. Physiology Normal values for arterial blood: pH = 7.37-7.43 (7.4) [H ] = 37-43 nanoeq/l (40) [HCO3 ] = 22-26 meq/l (24) pCO2= 35-45 mmHg (40) minimal tolerable pH = 6.8 maximal tolerable pH = 7.8 + -

  5. Cont’d These values are kept in normal or near normal range through 3 major mechanisms : 1.Chemical buffers: Intracellular & Extracellular 2.Ventilation: Increase or decrease blood CO2 3.Kidneys: Increase or decrease blood HCO3 -

  6. Review of acid-base homeostasis GUT Liver BONE Protein Fat, CHO CaCO3 H + HCO3 Ketoacid Lactic acid Glutamine CO2 PO4 NH4+ HCO3 HCO3 Daily excertion 15,000 mEq/d Daily excretion 60-80 mEq/d NH4+ TA +

  7. Proximal tubule and acid-base homeostasis

  8. Distal tubule and acid-base homeostasis

  9. Buffers • Buffers: Consist of weak acids. • Extra cellular buffers: 1.Bicarbonate: CO2 CO2+ H2O H2CO3 H + HCO3 [H ] = 24 *Advantages :Large amount Regulation of PCO2 by lungs - + (gas) (dis) PCO2 + HCO3

  10. Buffers NaHco3/H2co3+Hcl=H2co3+NacL NaHco3/H2co3+NaoH=NaHco3+H20

  11. Law of mass action: V1=V2 k1 [CO2] [H2O] = k2 [H+] [HO3-] K=[H+] [HCO3-] / [CO2] [H2O] K=[H+] [HCO3-] / [CO2]dis [H] =K [CO2] dis / [HCO3-] 37°C: K=800 [CO2]dis=0.03 PCO2 [H+] = 800 0.03 PCO2 / [HCO3-] [H ] = 24 PCO2 + - HCO3

  12. Cont’d 2.Inorganic Phosphate: Less important due to low amount (1 mmol/lit) 3.Plasma proteins: H + Pr HPr (pr/hpr) • Intracellular Buffers & Bone : 1.Proteins:Hemoglobin H + Hb HHb(Hb/HHb) 2.Bone: -Exchange of H with Na & K on the bone surface -Dissolving bone minerals Release of buffers - + - + + + +

  13. Pathophysiology • Acidemia , Alkalemia • Acidosis , Alkalosis • Metabolic , Respiratory Primary DiseaseCompensatory Response HCO3 (M. acidosis) PCO2 HCO3 (M. alkalosis) PCO2 PCO2 (R. alkalosis) HCO3 PCO2 (R. acidosis) HCO3 - - - -

  14. Predicted Compensation Disease Primary Compensation abnormality Met. acidosis 1meq/lit HCO3 1.2 mmHg PCO2 Met. alkalosis 1meq/lit HCO3 0.7mmHg PCO2 Resp. alkalosis 10mmHg PCO2 2 meq/lit HCO3 (acute) Resp. alkalosis 10mmHg PCO2 4 meq/lit HCO3 (chronic) Resp. acidosis 10mmHg PCO2 1 meq/lit HCO3 (acute) Resp. acidosis 10mmHg PCO2 3.5 meq/lit HCO3 (chronic)

  15. Other Equations - • Metabolic acidosis (Winter’s Formula): pCO2=1.5 [HCO3 ] + 8± 2 • Metabolic alkalosis : pCO2= 0.7[HCO3 ] + 21 ± 2 • Nomogram can also be used. -

  16. Respiratory acidosisAcute PH =7/40- 0.008(Paco2-40) Chronic PH = 7/40- 0.003(Paco2-40) Respiratory Alkalosis Acute PH =7/40+ 0.008(40-Paco2) Chronic PH = 7/40+ 0.003(40-Paco2)

  17. Are the measurements correct? + • Use the formula and these figures: pH [ H ] (nanomol/lit) 7.8 16 7.7 20 7.6 26 7.5 32 7.4 40 7.3 50 7.2 63 7.1 80 7.0 100 6.9 125 6.8 160  0.8  1.25

  18. Remember! - Blood pH [ H ] PCO2 [ HCO3 ] (nanoeq/lit) (mmHg) (meq/lit) Arterial 7.37-7.43 37-43 36-44 22-26 (7.4) (40) (40) (24) Venous 7.32-7.37 42-48 42-50 23-27 (7.35) (45) (46) (25) +

  19. Compensatory Response: 1 mmol/lit [HCO3 ] 1.2 mmHg pCO2 pCO2=1.5 [HCO3 ] + 8 ± 2 - -

  20. (Base excess)BE=-2,+2 (Buffer base)BB=42+BE

  21. Anion Gap • Anion Gap = Na - (Cl + HCO3) = UA – UC • Because Na + UC has to equal Cl + HCO3 + UA • Remember algebra? • UA = Unmeasured anions = albumin, phosphate, sulfate, lactate • UC = Unmeasured cations = Ca, K, Mg

  22. Low Anion Gap • Caused by decrease in UA • albuminuria secondary to nephrotic syndrome • Caused by increase in UC • Multiple myeloma (positively charged Ab’s)

  23. Concept of Anion Gap AG=8 AG=8 AG=16 HCO3 (24) HCO3 (16) HCO3 (16) Cl (108) Cl (116) Cl (108) Na (140) Na (140) Na (140)

  24. Metabolic Acidosis May be due to: 1.Increased production of acid: Lactic acidosis , Ketoacidosis , some poisonings e.g. salicylates 2.Decreased excretion of acid from kidneys: Decreased ammonia production (CRF) , RTA (type I or IV) 3.Alkali Loss: From GI tract (diarrhea) or Kidneys (type II RTA)

  25. Classification & Etiology - - + • According to anion gap: A.G.=[Na ] – ( [Cl ] + [HCO3 ] ) • High A.G. acidosis: Ketoacidosis , Lactic acidosis , Most poisonings , Renal failure • Normal A.G. acidosis: GI HCO3 loss (diarrhea) , Other renal disorders (RTA I , II and IV) , Ammonium chloride poisoning

  26. Clinical Manifestations & Rx • Clinical Manifestations: (MA) Kussmaul respiration , Fatigability , confusion , stupor , coma , decreased heart contractility , osteomalacia and rickets (long term) • Treatment: -Primary cause -If severe &/or symptomatic treat with alkali Needed NaHCO3=0.50 LBM(24- patient HCO3) -First give half of the needed NaHCO3 and calculate again.

  27. Quiz 1 A patient with diarrhea has the following ABG: pH=7.25 , HCO3=10 , PCO2=23 1.Are the measurements correct? 2.What is the acid-base disorder? + + 1.pH=7.25 [H ]=56.5 H = 24 pCO2/HCO3 H = 24 23.5/10 H = 55 So the measurement is correct. + + 2.pH=7.25 Acidosis ; Decreased HCO3 M.acidosis pCO2 should be=(1.5HCO3)+8±2=1.5 10 +8 ±2=23±2 So the disorder is simple M.acidosis.

  28. 10meq/lit HCO3 0.15meq PH10mmHg CO2 0.08meq PH Bicarbonate= BD( meq) . Kg 4

  29. Quiz PH=7.06 Paco2=50BE= -11 Hco3=18W=60Kg • 10 PCo2 0/08 PH • PH calculate=7.40-0.08=7.32 • PH-PHc=7.32- 7.06=0/26 • 10 Hco3 0/15 PH • BD=17 • 17 . 60 kg =255meq • 4

  30. Metabolic Alkalosis + • May be due to: 1.H Loss 2.HCO3 Retention 3.Volume Depletion (Contraction Alkalosis) • Compensatory response: 1meq/lit HCO3 0.7mmHg PCO2 -

  31. Quiz 2 • A patient with heart failure receiving diuretics has the following ABG: pH=7.46 , HCO3=30 , pCO2=45 What is the acid-base disorder? pH=7.46 Alkalosis Increased HCO3 M.Alkalosis pCO2 should be about =44.2 So the disorder is simple M.Alkalosis

  32. Why Metabolic Alkalosis? • In every patient with metabolic alkalosis there is a: 1.Precipitating cause 2. Continuing factor

  33. Etiology + • H Loss: 1.GI Loss:Vomiting or NG tube 2.Renal Loss: Diuretics , MC excess , Post chronic Hypercapnia , Milk-Alkali syndrome , High dose Carbenicilin 3.H shift into cells: Hypokalemia (<2 meq/lit) • HCO3 Retention: 1.Massive Blood Transfusion (>8 units) 2.Administration of NaHCO3 3.Milk-alkali syndrome • Contraction Alkalosis: 1.Diuretics 2.Cystic Fibrosis (sweat loss) 3.Achlorhydria (Gastric Loss) + -

  34. Why does Metabolic Alkalosis Continue? • Increased Bicarbonate Reabsorption due to: 1.Decreased GFR: decreased effective circulating volume) 2.Chloride depletion 3.Hypokalmia 4.Hyperaldosteronism • So you shall treat these factors in order to treat metabolic alkalosis.

  35. Clinical Manifestations • Clinical Manifestations: -Symptoms/Signs of Volume Depletion & hypokalemia -Lethargy , confusion and coma in severe cases -Tetany if hypocalcemia present

  36. Differential Diagnosis • Urine Cl <25 mmol/litUrine Cl >40 mmol/lit 1.Vomiting 1 M.C. Excess 2.Diuretics (late) 2.Diuretics (early) 3.Post hypercapnia 3.Alkali Load 4.Low Cl intake 4.Severe hypokalemia 5.Cystic fibrosis 5.Barter’s or 6.Fastidious diarrhea Giltleman’s syndrome

  37. Treatment • Saline responsive alkalosis: -Cases with urine Chloride< 25 meq/lit -Treat hpovolemia and Cl deficit with N/S -Also treat the primary cause such as vomiting • Saline resistant alkalosis: -Cases with urine Chloride >40 meq/lit and edematous states -Cases with edema:Useacetazolamide, HCl -If not effective and severe IV HCl can be used Needed HCl=50% Weight (Plasma HCO3 -24) -Treat the primary cause such as diuretic use

  38. Respiratory acidosisAcute H+/Paco2=0/7Chronic H+/Paco2=0/3 Respiratory Alkalosis Acute H+/Paco2=0/7 Chronic H+/Paco2=0/17

  39. Respiratory Acidosis • Due to decrease in effective ventilation. • Etiology: 1.Suppression of respiratory center: Drugs ,central apnea , cardiac arrest ,CNS disease (rare), Morbid obesity 2.Disorders of respiratory muscles and chest wall : Myasthenia Gravis, Hypokalemia , hypophosphatemia, Kyphoscoliosis, Spinal cord lesions, Morbid obesity 3.Disorders of upper respiratory tract: Layrgospasm, Foreign body, Obstructive sleep apnea 4.Defects in alveolar-capillary exchange:ARDS, Acute pulmonary edema, severe pneumonia, Pneumothorax, COPD, Morbid obesity,...

  40. Clinical Manifestations & Dx • Clinical manifestations: -Confusion to Coma in severe (pCO2>70) &/or acute cases -Vasodialation :Red eye and face -Increased ICP:Papilledema • Diagnosis: 1.Clinical manifestations 2.History (to differentiate acute from chronic ) 3.Degree of compensation: Resp. acidosis : 10 mmHg PCO2 1meq/lit HCO3 (acute) Resp. acidosis : 10 mmHg PCO2 3meq/lit HCO3 (chronic)

  41. Quiz 3 • A 20 yr old girl has attempted suicide with 200 mg of diazepam.She is in deep coma and has shallow respiration.ABG is as the following: pH=7.2 , pCO2=70 , HCO3=27 1.What is the acid-base disorder? 2.What would you expect HCO3 to be if it was a case of COPD? 1.The Hx is consistent with acute R. acidosis. So you expect 1 meq/lit rise of HCO3 for every 10 mmHg rise in pCO2 & 3 meq/l for 30 mmHg. The patient has pure R. acidosis. 2.In COPD we have chronic R. acidosis.So we expect about 3.5 meq/l rise in HCO3 for every 10 mmHg rise in pCO2 . HCO3 would be about 34. pH would be about 7.3

  42. Treatment 1.Correction of primary disease 2.Mechanical Ventilation in severe cases 3.Rapid infusion of bicarbonate in very severe cases such as cardio-pulmonary arrest

  43. Respiratory Alkalosis • Due to Increased ventilation • Etiology: I.Hypoxemia: Pneumonia, Acute asthma,Acute Pulmonary edema, Pulmonary fibrosis, Anemia 2.Stimulation of respiratory center: Anxiety, Fever, G sepsis, Salicylate poisoning, CNS disease (Tumor, Encephalitis), Cirrhosis, Pregnancy, After correction of metabolic acidosis 3.Mechanical ventilation (too much) -

  44. Clinical Manifestations & Dx • Hypoxemia stimulates respiratory center when pO2 is less than 50-60 mmHg. • In hypotention and anemia reduced O2 delivery to chemoreceptors of the great vessels stimulates respiratory center. • Clinical Manifestations: 1.Paresthesia to tetany 2.Stupor to coma 3.Asymptomatic in chronic cases

  45. Cont’d • Degree of compensation: R. alkalosis:10mmHg PCO2 2meq/lit HCO3 (acute) R. alkalosis:10 mmHg PCO2 4 meq/lit HCO3 (chronic) • Diagnosis:Clinical manifestations, History (acute vs chronic) & ABG • Treatment: 1.Primary Disorder 2.If symptomatic , breathing in a nylon bag

  46. Quiz 4 A 40 y/o cirrhotic man is brought to hospital with stupor ABG is as following: pH=7.46 , HCO3=20 , pCO2=30 What is the acid-base disorder? According to Hx, the patient has an underlying chronic disease precipitating to chronic R.alkalosis. 4-5 meq/L decrease in HCO3 is expected for every 10 mmHg decrease in pCO2. So the patient has pure R. alkalosis

  47. Cont’d The patient develops oliguria & hypotension on the next day.ABG changes as follows: pH=7.38 , HCO3=13, pCO2=25 What is the acid-base disorder now? The patient has normal pH with decreased pCO2 & HCO3.So there should be a mixed acid-base disorder. According to Hx chronic R. alkalosis is expected. But the decrease in HCO3 is more than expected (18).So there is also M.acidosis which is explained by hypotension & oliguria.

  48. Mixed acid-base disorders I.M. acidosis & R. acidosis: 1.Cardio-pulmonary arrest 2.Severe pulmonary edema 3.Poisoning with both salicylate & a sedative drug 4.Renal Failure with COPD II.M. acidosis & R. alkalosis: 1.Salicylate poisoning 2.Severe sepsis 3.Combined renal & hepatic failure 4.Ethanol Toxicity

  49. Cont’d III.M. alkalosis & R. alkalosis: 1.Pregnancy with vomiting 2.Chronic liver disease on diuretic therapy IV.M. alkalosis & R. acidosis: Seen in COPD with : 1.Diuretics 2.Steroids 3.Vomiting 4.To much ventilatory support V.M. acidosis & M. alkalosis:Seen in vomiting with: 1.Renal failure 2.Alcoholic or diabetic ketoacidosis *Only R. alkalosis & R. acidosis can not happen together.

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