Acid Base Disturbance

Total Page:16

File Type:pdf, Size:1020Kb

Acid Base Disturbance 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.
Recommended publications
  • Severe Metabolic Acidosis in a Patient with an Extreme Hyperglycaemic Hyperosmolar State: How to Manage? Marloes B
    Clinical Case Reports and Reviews Case Study ISSN: 2059-0393 Severe metabolic acidosis in a patient with an extreme hyperglycaemic hyperosmolar state: how to manage? Marloes B. Haak, Susanne van Santen and Johannes G. van der Hoeven* Department of Intensive Care Medicine, Radboud University Medical Center, Nijmegen, the Netherlands Abstract Hyperglycaemic hyperosmolar state (HHS) and diabetic ketoacidosis (DKA) are often accompanied by severe metabolic and electrolyte disorders. Analysis and treatment of these disorders can be challenging for clinicians. In this paper, we aimed to discuss the most important steps and pitfalls in analyzing and treating a case with extreme metabolic disarrangements as a consequence of an HHS. Electrolyte disturbances due to fluid shifts and water deficits may result in potentially dangerous hypernatriema and hyperosmolality. In addition, acid-base disorders often co-occur and several approaches have been advocated to assess the acid-base disorder by integration of the principles of mass balance and electroneutrality. Based on the case vignette, four explanatory methods are discussed: the traditional bicarbonate-centered method of Henderson-Hasselbalch, the strong ion model of Stewart, and its modifications ‘Stewart at the bedside’ by Magder and the simplified Fencl-Stewart approach. The four methods were compared and tested for their bedside usefulness. All approaches gave good insight in the metabolic disarrangements of the presented case. However, we found the traditional method of Henderson-Hasselbalch and ‘Stewart at the bedside’ by Magder most explanatory and practical to guide treatment of the electrolyte disturbances and in exploring the acid-base disorder of the presented case. Introduction This is accompanied by changes in pCO2 and bicarbonate (HCO₃ ) levels, depending on the cause of the acid-base disorder.
    [Show full text]
  • Arterial Blood Gases: Acid-Base Balance
    EDUCATIONAL COMMENTARY – ARTERIAL BLOOD GASES: ACID-BASE BALANCE Educational commentary is provided through our affiliation with the American Society for Clinical Pathology (ASCP). To obtain FREE CME/CMLE credits click on Earn CE Credits under Continuing Education on the left side of the screen. **Florida licensees, please note: This exercise will appear in CE Broker under the specialty of Blood Gas Analysis. LEARNING OUTCOMES On completion of this exercise, the participant should be able to • identify the important buffering systems in the human body. • explain the Henderson-Hasselbalch equation and its relationship to the bicarbonate/carbonic acid buffer system. • explain the different acid-base disorders, causes associated with them, and compensatory measures. • evaluate acid-base status using patient pH and pCO2 and bicarbonate levels. Introduction Arterial blood gas values are an important tool for assessing oxygenation and ventilation, evaluating acid- base status, and monitoring the effectiveness of therapy. The human body produces a daily net excess of acid through normal metabolic processes: cellular metabolism produces carbonic, sulfuric, and phosphoric acids. Under normal conditions, the body buffers accumulated hydrogen ions (H+) through a variety of buffering systems, the respiratory center, and kidneys to maintain a plasma pH of between 7.35 and 7.45. This tight maintenance of blood pH is essential: even slight changes in pH can alter the functioning of enzymes, the cellular uptake and use of metabolites, and the uptake and release of oxygen. Although diagnoses are made by physicians, laboratory professionals must be able to interpret arterial blood gas values to judge the validity of the laboratory results they report.
    [Show full text]
  • TITLE: Acid-Base Disorders PRESENTER: Brenda Suh-Lailam
    TITLE: Acid-Base Disorders PRESENTER: Brenda Suh-Lailam Slide 1: Hello, my name is Brenda Suh-Lailam. I am an Assistant Director of Clinical Chemistry and Mass Spectrometry at Ann & Robert H. Lurie Children’s Hospital of Chicago, and an Assistant Professor of Pathology at Northwestern Feinberg School of Medicine. Welcome to this Pearl of Laboratory Medicine on “Acid-Base Disorders.” Slide 2: During metabolism, the body produces hydrogen ions which affect metabolic processes if concentration is not regulated. To maintain pH within physiologic limits, there are several buffer systems that help regulate hydrogen ion concentration. For example, bicarbonate, plasma proteins, and hemoglobin buffer systems. The bicarbonate buffer system is the major buffer system in the blood. Slide 3: In the bicarbonate buffer system, bicarbonate, which is the metabolic component, is controlled by the kidneys. Carbon dioxide is the respiratory component and is controlled by the lungs. Changes in the respiratory and metabolic components, as depicted here, can lead to a decrease in pH termed acidosis, or an increase in pH termed alkalosis. Slide 4: Because the bicarbonate buffer system is the major buffer system of blood, estimation of pH using the Henderson-Hasselbalch equation is usually performed, expressed as a ratio of bicarbonate and carbon dioxide. Where pKa is the pH at which the concentration of protonated and unprotonated species are equal, and 0.0307 is the solubility coefficient of carbon dioxide. Four variables are present in this equation; knowing three variables allows for calculation of the fourth. Since pKa is a constant, and pH and carbon dioxide are measured during blood gas analysis, bicarbonate can, therefore, be determined using this equation.
    [Show full text]
  • Approach to Acute Kidney Injury: Differentiation of Prerenal, Postrenal and Intrinsic Renal Disease, Acute Tubular Necrosis and Renal Vascular Disease
    Acute Kidney Injury, Renal Vascular Disease Renal Genital Urianry System 2019 APPROACH TO ACUTE KIDNEY INJURY: DIFFERENTIATION OF PRERENAL, POSTRENAL AND INTRINSIC RENAL DISEASE, ACUTE TUBULAR NECROSIS AND RENAL VASCULAR DISEASE Biff F. Palmer, MD, Office: H5.112; Phone 87848 Email: [email protected] LEARNING OBJECTIVES • Given laboratory tests results and radiographic imaging, be able to diagnose a patients with an increased serum creatinine concentration as having post-renal renal disease and list the common clinical etiologies of urinary obstruction • Given laboratory tests results and radiographic imaging, be able to diagnose a patients with an increased serum creatinine concentration as having pre-renal kidney injury • Given pertinent aspects of the history, physical examination, serum and urine electrolytes, and urinalysis in any patient, be able to distinguish pre-renal renal failure from intrinsic renal disease • Given urine and plasma concentrations of sodium and creatinine in any patient, be able to calculate the fractional excretion of sodium (FENa) and interpret the results • List the renal syndromes associated with use of NSAID’s • List the characteristics of thromboembolic disease of the kidney, multiple choesterol emboli syndrome, renal vein thrombosis, and renal artery stenosis After determining chronicity and assessing the level of renal function, one should attempt to classify the patient with renal disease into one of several syndromes based on the renal structures most affected: pre-renal, post-renal or intrinsic renal disease. This classification is based on the information obtained in the history, physical examination, laboratory tests and selected imaging studies. It is particularly important to identify prerenal and postrenal disorders because theses disorders are often readily reversible.
    [Show full text]
  • Problem-Based Review: a Patient with Metabolic Acidosis
    Acute Medicine 2012 11(4): 251-256 251 Trainee Section Problem-Based Review: A patient 251 with metabolic acidosis saf R Allan & C Foster Abstract Metabolic acidosis is a common metabolic derangement present in the acute medical patient. A thorough and structured investigative approach is required as there are many causes and management is reliant on identifying these. In particular calculation of the anion gap with correction for albumin level and use of the delta ratio can be helpful in complex cases especially in patients where a combination of metabolic derangements may be present. Keywords metabolic acidosis, anion gap, delta ratio, renal tubular acidosis, bicarbonate Key points • Calculation of the anion gap is crucial in identifying the cause of metabolic acidosis. • Metabolic acidosis is often multi-factorial and the delta ratio calculation can be useful in identifying situations where a normal gap acidosis coexists with a raised anion gap cause. • Identification of the specific cause(s) of metabolic acidosis is vital as this will usually guide treatment. • Bicarbonate treatment has a role in some cases but adverse effects should be considered. Case Vignette Although the anion gap calculation will narrow A 37 year old male with no past medical history presents our differential (Table 2), many possible explanations to the acute medical unit (AMU) with a history of general for the acidosis remain, especially when the gap is deterioration in health over the last 8 months. He has lost 10 high. The mnemonic MUDPILERS (Methanol, kg of weight and has severe fatigue. More recently he describes a Uraemia, Diabetic Ketoacidosis or other causes Table 1.
    [Show full text]
  • PHAR 503 Exam 2
    PHAR 503 Exam 2 Rho Chi Acid-Base Disorders Which medication would most likely NOT lead to a metabolic alkalosis? A. Loop Diuretic B. Thiazide Diuretic C. Desmopressin D. Citrate Which medication would most likely NOT lead to a metabolic alkalosis? A. Loop Diuretic B. Thiazide Diuretic C. Desmopressin D. Citrate Diuretics increase loss of H+, vomiting, hypokalemia, citrate is metabolized to HCO3- A patient suffering from an acute panic attack might be at risk for developing: A. Respiratory alkalosis B. Metabolic alkalosis C. Respiratory Acidosis D. Metabolic Acidosis A patient suffering from an acute panic attack might be at risk for developing: A. Respiratory alkalosis B. Metabolic alkalosis C. Respiratory Acidosis D. Metabolic Acidosis Hyperventilating -> blowing off CO2 (acid) If you have a patient who is experiencing a respiratory acidosis, which of the following sets of labs would most likely match the patient? A. pH: 7.41, HCO3-: 20 B. pH: 7.35, CO2: 52 C. pH: 7.35, HCO3-: 20 D. pH: 7.45, CO2: 32 If you have a patient who is experiencing a respiratory acidosis, which of the following sets of labs would most likely match the patient? A. pH: 7.41, HCO3-: 20 B. pH: 7.35, CO2: 52 C. pH: 7.35, HCO3-: 20 D. pH: 7.45, CO2: 32 Metabolic: HCO3- abnormalities, respiratory: PaCO2 What is the normal range for PaCO2? What is the normal range for HCO3-? What is the normal range for PaCO2? 35-45 (40!) What is the normal range for HCO3-? 22-26 (24!) ROME Respiratory Opposite: PaCo2 and pH go in opposite directions Metabolic Equal: HCO3- and pH go in the same direction Which of the following would NOT cause a metabolic acidosis? A.
    [Show full text]
  • Diabetic Ketoalkalosis in Children and Adults
    Original Article Diabetic Ketoalkalosis in Children and Adults Emily A. Huggins, MD, Shawn A. Chillag, MD, Ali A. Rizvi, MD, Robert R. Moran, PhD, and Martin W. Durkin, MD, MPH and DR are calculated because the pH and bicarbonate may be near Objectives: Diabetic ketoacidosis (DKA) with metabolic alkalosis normal or even elevated. In addition to having interesting biochemical (diabetic ketoalkalosis [DKALK]) in adults has been described in the features as a complex acid-base disorder, DKALK can pose diagnostic literature, but not in the pediatric population. The discordance in the and/or therapeutic challenges. change in the anion gap (AG) and the bicarbonate is depicted by an Key Words: delta ratio, diabetic ketoacidosis, diabetic ketoalkalosis, elevated delta ratio (DR; rise in AG/drop in bicarbonate), which is metabolic alkalosis normally approximately 1. The primary aim of this study was to de- termine whether DKALK occurs in the pediatric population, as has been seen previously in the adult population. The secondary aim was iabetic ketoacidosis (DKA), a common and serious dis- to determine the factors that may be associated with DKALK. Dorder that almost always results in hospitalization, is de- Methods: A retrospective analysis of adult and pediatric cases with a fined by the presence of hyperglycemia, reduced pH, metabolic 1 primary or secondary discharge diagnosis of DKA between May 2008 and acidosis, elevated anion gap (AG), and serum or urine ketones. August 2010 at a large urban hospital was performed. DKALK was as- In some situations, a metabolic alkalosis coexists with DKA sumedtobepresentiftheDRwas91.2 or in cases of elevated bicarbonate.
    [Show full text]
  • Acid-Base Physiology & Anesthesia
    ACID-BASE PHYSIOLOGY & ANESTHESIA Lyon Lee DVM PhD DACVA Introductions • Abnormal acid-base changes are a result of a disease process. They are not the disease. • Abnormal acid base disorder predicts the outcome of the case but often is not a direct cause of the mortality, but rather is an epiphenomenon. • Disorders of acid base balance result from disorders of primary regulating organs (lungs or kidneys etc), exogenous drugs or fluids that change the ability to maintain normal acid base balance. • An acid is a hydrogen ion or proton donor, and a substance which causes a rise in H+ concentration on being added to water. • A base is a hydrogen ion or proton acceptor, and a substance which causes a rise in OH- concentration when added to water. • Strength of acids or bases refers to their ability to donate and accept H+ ions respectively. • When hydrochloric acid is dissolved in water all or almost all of the H in the acid is released as H+. • When lactic acid is dissolved in water a considerable quantity remains as lactic acid molecules. • Lactic acid is, therefore, said to be a weaker acid than hydrochloric acid, but the lactate ion possess a stronger conjugate base than hydrochlorate. • The stronger the acid, the weaker its conjugate base, that is, the less ability of the base to accept H+, therefore termed, ‘strong acid’ • Carbonic acid ionizes less than lactic acid and so is weaker than lactic acid, therefore termed, ‘weak acid’. • Thus lactic acid might be referred to as weak when considered in relation to hydrochloric acid but strong when compared to carbonic acid.
    [Show full text]
  • Hyperkalemia: This Time, Not the Usual Suspect
    TUBULAR QUIZ Port J Nephrol Hypert 2018; 32(4): 395-397 • Advance Access publication 4 January 2019 Hyperkalemia: this time, not the usual suspect Anna Lima, Pedro Campos, Ana Gaspar, Afonso Santos, Patricia Carrilho Department of Nephrology, Hospital Prof Dr Fernando Fonseca, Lisbon, Portugal Received for publication: Dec 18, 2018 Accepted in revised form: Jan 4, 2019 A 49-year-old Caucasian male was admitted to the acidosis, one important step to search for the cause is emergency department with a three-day history of to calculate the anion gap.1 In this case the anion gap abdominal pain and nausea. These episodes were fre- was normal (AG= Na – (CL+HCO3) =12mmol/L). The next quent and, in the previous four months, he had noticed step was to calculate the urinary anion gap (UAG= (Na+ fatigue, more severe in the lower limbs, and symptoms + K+) – Cl-= 74mmol/L), which was highly positive. So, compatible with postural hypotension. He had no fever we were in presence of a metabolic acidosis with non- or any other symptoms. Lab tests requested by his increased anion gap, positive UAG, hyperkalemia and general practitioner six weeks earlier had revealed acidic urine (pH 5) in a patient with normal renal function hyperkalemia, without other relevant changes. He had matching a type IV (distal) renal tubular acidosis.2 followed a low-potassium diet since then. Past medical history included active smoking habits, intravenous There are many causes for hyperkalemic distal renal drug use (he suspended seventeen years ago), and tubular acidosis, the most common of which is diabetes changed bowel habits with alternating obstipation and mellitus (by definition a hyporeninemic hypoaldoster- diarrhea.
    [Show full text]
  • ABG Analysis in Clinical Setting
    CHAPTER ABG Analysis in Clinical Setting 117 Rajesh Mahajan, Suman Sethi INTRODUCTION defined by the ratio of PCO2 to HCO3 and not by absolute Acid-Base balance is an intricate concept which requires an value of either one alone.5,6 intimate and detailed knowledge of the body’s metabolic Overview of Fundamentals of Acid-Base Disorder pathways used to eliminate the H+ ion. Accurately Normal metabolism of proteins and nucleotides generates interpreting acid-base balance requires simultaneous about 100 mmol H+ per day in the form of sulphuric and measurements of arterial pH and plasma electrolytes, phosphoric acids. By comparison, hydration of CO2 to as well as knowledge of compensatory physiologic form H CO generates 12,500 mmol H+ per day. mechanisms. In this article, we’ll review normal acid-base 2 3 physiology, acid-base disturbances, and lab techniques Carbon dioxide transport and mathematical calculations used to identify the cause 1. Transport of carbon dioxide in the blood is of acid-base derangements. considerably more complex. A small portion of carbon dioxide, about 5 percent, remains BASIC PHYSIOLOGY unchanged and is transported dissolved in blood. Acid-base Chemistry 2. The remainder is found in reversible chemical pH combinations in red blood cells or plasma. Some The concept of pH was put forward by the Danish chemist, carbon dioxide binds to blood proteins, principally Soren Peter Sorensen in 1909 to refer to the negative hemoglobin, to form a compound known as logarithm of hydrogen ion (H+) concentration. An increase carbamate. in the pH indicates a proportionate decrease in the 3., About 88 percent of carbon dioxide in the blood is [H+] and a decrease in the pH indicates a proportionate in the form of bicarbonate ion.
    [Show full text]
  • 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].
    [Show full text]
  • 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.
    [Show full text]