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Acid Base Disturbance

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Acid Base Disturbance ภูษิตภูษิต เฟเฟองฟองฟู ู พบพบ.. วววว..ศัศัลยศาตรลยศาตรทั่ทั่วไปวไป,, วววว..เวชบเวชบําบําบัดวัดวิกฤติกฤต กองศกองศัลยกรรมัลยกรรม โรงพยาบาลพระโรงพยาบาลพระมงกมงกุฏุฏเกลเกลาา Overview z BodyBody BufferBuffer SystemSystem z AcidAcid BaseBase disturbancesdisturbances z TreatmentTreatment Definition z AcidsAcids releaserelease HH+ z example:example: HClHCl -->> HH+ ++ ClCl- z BasesBases absorbabsorb HH+ - + z example:example: HCOHCO3 ++ HH -->> HH2COCO3 Introduction z MetabolismMetabolism generatesgenerates HydrogenHydrogen ionsions 4040-- 8080 mmolmmol/day/day z pHpH 7.357.35--7.467.46 retainedretained HH+ withinwithin 3535--4545 nmol/lnmol/l H+ per day = 40-80 x 1,000,000 nmol/l pH is logarithmic z pHpH == loglog 1/[H1/[H+]] == -- loglog [H[H+]] == -- loglog 0.000000040.00000004 EqEq/L/L pHpH == 7.47.4 SmallSmall ΔΔpHpH meansmeans pHpH 7.47.4 == 0.000000040.00000004 largelarge ΔΔ[H[H++]] pHpH 7.17.1 == 0.000000080.00000008 Buffer: pH Guardian H+ Load Distribution and extra- Cellular Cell Respiratory buffering buffering compensation 100 Renal H+ secretion 50 0 61224 72 Hours The ECF accounted for ~43% of total buffering Carbonic acid-Bicarbonate Buffer System - + CO2 + H2O H2CO3 HCO3 + H CO2 Production Dietary protein breakdown 14,000-20,000 mM/day 40-80 mEq/day 40 mmHg [H+] = 24 x pCO2 - [HCO3 ] 40 nEq/L 24 mEq/L 40 mmHg [H+] = 24 x pCO2 - [HCO3 ] 40 nEq/L 24 mEq/L estimated[H+] pH 70 7.10 60 7.20 50 7.30 40 7.40 30 7.50 estimated[H+] pH 70 7.10 60 7.20 CO =11.2 2 50 7.30 + 10 H+ - HCO3 = 14 pH = 6.20 40 7.40 30 7.50 + 10 CO2 lost CO2 = 1.2 - HCO3 = 24 pH = 7.40 CO =1.2 2 CO2 =0.9 - - HCO3 = 14 HCO3 = 14 pH = 7.17 pH = 7.29 Open Compensated Henderson-Hasselbach Equation - + CO2 + H2O H2CO3 HCO3 + H - pH =pK+log [A ] [HA] [HA] = [H2CO3 ] (at equilibrium) = [CO2]dissolved - pH = 6.1 +l og [HCO3 ] [CO2]dissolved SCO2 = 0.03 mmoles CO2/L/mmHg [HCO -] pH = 6.1 +log 3 SCO2 x PCO2 [HCO -] pH = 6.1 +log 3 0.03 x PCO2 pH =pK+log Kidneys Lungs CO2 [Kidney] pH ~ ~ [Lung] - + HCO3 + H - + HCO3 H : Phosphoric + acid, NH4 Respiratory Component PaCO2 & Minute Ventilation PaCO2 PaCO2 = 0.8 VCO2 RR(Vt-Vd) 40 Minute Ventilation Renal Component z Production of “new” bicarbonate via excretion of acid ≈ 70 mEq/day z Reabsorption of filtered bicarbonate ≈ 4,000 mEq/day Acid-base disturbances from Gastrointestinal loss Vomiting: Loss of H+ leading to alkalosis Highly acidic, pH =1.0 - Secretes HCO3 Diarrhea: pH varies from - Loss of HCO3 leading to 4.0 to 8.0 acidosis The Big 3 of pH Guardian H+ Load Distribution and extra- Cellular Cell Respiratory buffering buffering compensation 100 Renal H+ secretion 50 0 61224 72 Hours The Four Cardinal Acid Base Disorders - Disorder pH pCO2 [HCO3 ] M acidosis ↓↓↓ M alkalosis ↑↑↑ R acidosis ↓ ↑ ↑ R alkalosis ↑ ↓ ↓ Boston approach in Systemic ABG analysis 1.1. CheckCheck arterialarterial pHpH - 22.. [[HCOHCO3 ]] && PaCOPaCO2 analysisanalysis 3.3. CalculateCalculate AGAG 4.4. AssessAssess deltadelta ratioratio 5.5. CheckCheck ““cluesclues”” 6.6. AssessAssess compensatorycompensatory responsesresponses 77.. FormulateFormulate acidacid--basebase diagnosisdiagnosis 1. Check arterial pH z pH < 7.4 = acidosis pH > 7.4 = alkalosis z Principle – No over-compensation Boston approach in Systemic ABG analysis √ 1.1. CheckCheck arterialarterial pHpH - 22.. [[HCOHCO3 ]] && PaCOPaCO2 analysisanalysis 3.3. CalculateCalculate AGAG 4.4. AssessAssess deltadelta ratioratio 5.5. CheckCheck ““cluesclues”” 6.6. AssessAssess compensatorycompensatory responsesresponses 7.7. FormulateFormulate acidacid--basebase diagnosisdiagnosis - 2. [HCO3 ]& PaCO2 analysis Respiratory Compensation for Metabolic Changes z Metabolic acidosis - PaCO2 decreases by 1.2 x the drop in [HCO3 ] - PaCO2 ≈≈ 1.51.5 [HCO[HCO3 ]] ++ 88 z Metabolic alkalosis - PaCO2 increases by 0.7 x the rise in [HCO3 ] - PaCO2 ≈ 0.9 [HCO3 ] + 16 Metabolic Compensation for Respiratory Changes z Respiratory Acidosis - Acute: [HCO3 ] increases by 0.1 x the rise in PaCO2 - Chronic: [HCO3 ] increases by 0.35 x the rise in PaCO2 z Respiratory Alkalosis - Acute: [HCO3 ] decreases by 0.2 x the fall in PaCO2 - Chronic: [HCO3 ] decreases by 0.5 x the fall in PaCO2 - [HCO3 ]& PaCO2 analysis z Both are low The last 2-digit if pH = PaCO2 metabolic acidosis respiratory alkalosis Both are high metabolic alkalosis respiratory acidosis - z Opposite directions [HCO3 ]& PaCO2 Mixed disorder must be present • 60-year-old diabetic with a long history of not taking her insulin. She is admitted to the hospital and you receive the following data on her: - pH 7.26, PaCO2 42, HCO3 17... Metabolic acidosis. • A 1st year resident was anxious about her basic sciences examination. She felt numbness around her mouth and tingling in her hands and went to the clinic. - pH 7.48, PaCO2 30, HCO3 23… Respiratory alkalosis A 1st year medical student who did really well on his 1st biochemistry test celebrated too much afterwards. After a weekend of atonement, his lab values are: - pH 7.48, PaCO2 51, HCO3 29… Metabolic alkalosis A 40 year-old man with renal failure for 1 year presents with nausea, vomiting and weakness. His blood chemistry reveals Na 138 mEq/L, K 5.5 mEq/L, Cl 95 mEq/L, HCO3 16 mEq/L ABG: pH 7.31, PaCO2 31 mmHg The most likely acid-base disorder is A. Metabolic alkalosis B. Respiratory alkalosis C. Mixed respiratory alkalosis and metabolic acidosis D. Metabolic acidosis E. Mixed respiratory acidosis and metabolic alkalosis A 40 year-old man with renal failure for 1 year presents with nausea, vomiting and weakness. His blood chemistry reveals Na 138 mEq/L, K 5.5 mEq/L, Cl 95 mEq/L, HCO3 16 mEq/L ABG: pH 7.31, PaCO2 31 mmHg The most likely acid-base disorder is A. Metabolic alkalosis B. Respiratory alkalosis C. Mixed respiratory alkalosis and metabolic acidosis D. Metabolic acidosis E. Mixed respiratory acidosis and metabolic alkalosis - Winter’s formula: PaCO2 = 1.5 [HCO3 ] + 8 = 1.5[16] + 8 = 32 AnAn acutelyacutely--illill 5050--yearyear--oldold womanwoman withwith aa historyhistory ofof severesevere vomitingvomiting forfor thethe pastpast 44 days.days. PhysicalPhysical examinationexamination profoundprofound lethargy,lethargy, aa pulsepulse raterate ofof 120/min,a120/min,a respirationrespiration raterate ofof 12/min,12/min, andand BPBP ofof 80/5080/50 mmHg.mmHg. SerumSerum electrolyteselectrolytes SodiumSodium 140140 meqmeq/L/L PotassiumPotassium 3.33.3 meqmeq/L/L ChlorideChloride 8585 meqmeq/L/L BicarbonateBicarbonate 2525 meqmeq/L/L ArterialArterial bloodblood studiesstudies onon roomroom air:air: pHpH 7.407.40 1 PaCOPaCO2 4141 mmHg,mmHg, AnAn acutelyacutely--illill 5050--yearyear--oldold womanwoman withwith aa historyhistory ofof severesevere vomitingvomiting forfor thethe pastpast 44 days.days. PhysicalPhysical examinationexamination profoundprofound lethargy,lethargy, aa pulsepulse raterate ofof 120/min,a120/min,a respirationrespiration raterate ofof 12/min,12/min, andand BPBP ofof 80/5080/50 mmHg.mmHg. SerumSerum electrolyteselectrolytes SodiumSodium 140140 meqmeq/L/L PotassiumPotassium 3.33.3 meqmeq/L/L ChlorideChloride 8585 meqmeq/L/L BicarbonateBicarbonate 2525 meqmeq/L/L 2 ArterialArterial bloodblood studiesstudies onon roomroom air:air: pHpH 7.407.40 PaCOPaCO2 4141 mmHg,mmHg, 1 Boston approach in Systemic ABG analysis √ 1.1. CheckCheck arterialarterial pHpH √ - 22.. [[HCOHCO3 ]] && PaCOPaCO2 analysisanalysis 3.3. CalculateCalculate AGAG 4.4. AssessAssess deltadelta ratioratio 5.5. CheckCheck ““cluesclues”” 6.6. AssessAssess compensatorycompensatory responsesresponses 7.7. FormulateFormulate acidacid--basebase diagnosisdiagnosis 3. Calculate “Anion Gap” z Unmeasured cations UC UA K+, Ca++, and Mg++ account for about 11 mEq/L. AG z Unmeasured anions 3- 2- HCO - (PO4) , SO4 , albumin and some 3 organic acids, accounting for 20 to 24 mEq/L. Na+ z Typical anion gap is 23 − 11 = 12 mEq/L. z The anion gap can be affected by increases or decreases in the UC or UA. Cl- Decreased anion gap UC UA z ↑ Unmeasured cations K+, Ca++, and Mg++ AG gamma globulin HCO - z ↓ Unmeasured anions 3 (PO4)3- , SO42-, albumin and some organic acids, + Na z The effect of low albumin can be accounted for by adjusting the normal - range for the anion gap 2.5 mEq/L Cl upward for every 1-g/dL fall in albumin. Normal anion gap Metabolic acidosis ~ 10-12 mEq/L ≡ [Na+] - ([Cl-] + [HCO -]) AG 3 HCO - - 3 HCO loss 3 Na+ = Normal AG Metabolic acidosis • Occur in GI tract or Renal Cl- Causes of a “Normal anion gap” (hyperchloremic) metabolic acidosis 1. GI bicarbonate loss: diarrhea villous adenoma pancreatic fistulae uretero-sigmoidostomy obstructed uretero-ileostomy 2. Renal bicarbonate (or equivalent) loss proximal RTA, distal RTA and type IV RTA early renal failure 3. Ingestions & infusions ammonium chloride hyperalimentation (arginine/lysine-rich) - Diarrhea Causes Loss of HCO3 Normal Diarrhea Pancreas Pancreas HCO - HCO - 3 Ileum 3 - HCO3 Ileum Cl- Cl- - Colon + - Colon Cl K HCO3 Normal AG acidosis and Hypo-K Pancreatic fistula or transplant Pancreas - HCO3 Ileum Cl- Skin or urinary bladder Obstructed Uretero-ileostomy Skin - Ureter HCO3 Cl- Cl- Ileal loop Obstructed ileal loop Wide-anion gap Metabolic acidosis ~ 10-12 mEq/L ≡ [Na+] - ([Cl-] + [HCO -]) AG 3 A- เติมกรด HA → H+ + A- HCO - 3 • Organic acid load: Shock, Renal Na+ failure, DKA • Toxic ingextation: ASA, Alcohol etc. Cl- = Wide AG Metabolic acidosis ~ 10-12 mEq/L ≡ [Na+] - ([Cl-] + [HCO -]) AG 3 A- - • AG elevated HCO3 Na+ in either acidosis or alkalosis • AG > 20 Cl- 67% likelihood of metabolic acidosis • AG > 30 ~ 100% likelihood of metabolic acidosis AnAn acutelyacutely--illill 5050--yearyear--oldold womanwoman withwith aa historyhistory ofof severesevere vomitingvomiting forfor thethe pastpast 44 days.days. PhysicalPhysical examinationexamination profoundprofound lethargy,lethargy, aa pulsepulse raterate ofof 120/min,a120/min,a respirationrespiration raterate ofof 12/min,12/min, andand BPBP ofof 80/5080/50 mmHg.mmHg. SerumSerum electrolyteselectrolytes SodiumSodium 140140 meqmeq/L/L PotassiumPotassium 3.33.3 meqmeq/L/L ChlorideChloride 8585 meqmeq/L/L BicarbonateBicarbonate 2525 meqmeq/L/L 2 ArterialArterial bloodblood studiesstudies onon roomroom air:air: pHpH 7.407.40 PaCOPaCO2 4141 mmHg,mmHg, 1 3.
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  • Acid-Base Disorders in Patients with Chronic Obstructive Pulmonary Disease: a Pathophysiological Review

    Acid-Base Disorders in Patients with Chronic Obstructive Pulmonary Disease: a Pathophysiological Review

    Hindawi Publishing Corporation Journal of Biomedicine and Biotechnology Volume 2012, Article ID 915150, 8 pages doi:10.1155/2012/915150 Review Article Acid-Base Disorders in Patients with Chronic Obstructive Pulmonary Disease: A Pathophysiological Review Cosimo Marcello Bruno and Maria Valenti Department of Internal Medicine and Systemic Diseases, University of Catania, 95100 Catania, Italy Correspondence should be addressed to Cosimo Marcello Bruno, [email protected] Received 29 September 2011; Accepted 26 October 2011 Academic Editor: Saulius Butenas Copyright © 2012 C. M. Bruno and M. Valenti. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The authors describe the pathophysiological mechanisms leading to development of acidosis in patients with chronic obstructive pulmonary disease and its deleterious effects on outcome and mortality rate. Renal compensatory adjustments consequent to acidosis are also described in detail with emphasis on differences between acute and chronic respiratory acidosis. Mixed acid-base disturbances due to comorbidity and side effects of some drugs in these patients are also examined, and practical considerations for a correct diagnosis are provided. 1. Introduction However, an alteration in respiratory exchanges, as occurs in advanced phase of COPD, results in retention of CO2. Chronic obstructive pulmonary disease (COPD) is a major Carbon dioxide is then hydrated with the formation of public health problem. Its prevalence varies according to carbonic acid that subsequently dissociates with release of country, age, and sex. On the basis of epidemiologic data, hydrogen ions (H+) in the body fluids according to the fol- the projection for 2020 indicates that COPD will be the lowing equation: third leading cause of death worldwide and the fifth leading − + cause of disability [1].
  • PGE2 EP1 Receptor Inhibits Vasopressin-Dependent Water

    PGE2 EP1 Receptor Inhibits Vasopressin-Dependent Water

    Laboratory Investigation (2018) 98, 360–370 © 2018 USCAP, Inc All rights reserved 0023-6837/18 PGE2 EP1 receptor inhibits vasopressin-dependent water reabsorption and sodium transport in mouse collecting duct Rania Nasrallah1, Joseph Zimpelmann1, David Eckert1, Jamie Ghossein1, Sean Geddes1, Jean-Claude Beique1, Jean-Francois Thibodeau1, Chris R J Kennedy1,2, Kevin D Burns1,2 and Richard L Hébert1 PGE2 regulates glomerular hemodynamics, renin secretion, and tubular transport. This study examined the contribution of PGE2 EP1 receptors to sodium and water homeostasis. Male EP1 − / − mice were bred with hypertensive TTRhRen mice (Htn) to evaluate blood pressure and kidney function at 8 weeks of age in four groups: wildtype (WT), EP1 − / − , Htn, HtnEP1 − / − . Blood pressure and water balance were unaffected by EP1 deletion. COX1 and mPGE2 synthase were increased and COX2 was decreased in mice lacking EP1, with increases in EP3 and reductions in EP2 and EP4 mRNA throughout the nephron. Microdissected proximal tubule sglt1, NHE3, and AQP1 were increased in HtnEP1 − / − , but sglt2 was increased in EP1 − / − mice. Thick ascending limb NKCC2 was reduced in the cortex but increased in the medulla. Inner medullary collecting duct (IMCD) AQP1 and ENaC were increased, but AVP V2 receptors and urea transporter-1 were reduced in all mice compared to WT. In WT and Htn mice, PGE2 inhibited AVP-water transport and increased calcium in the IMCD, and inhibited sodium transport in cortical collecting ducts, but not in EP1 − / − or HtnEP1 − / − mice. Amiloride (ENaC) and hydrochlorothiazide (pendrin inhibitor) equally attenuated the effect of PGE2 on sodium transport. Taken together, the data suggest that EP1 regulates renal aquaporins and sodium transporters, attenuates AVP-water transport and inhibits sodium transport in the mouse collecting duct, which is mediated by both ENaC and pendrin-dependent pathways.