Pravin Pawal Abg


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Pravin Pawal Abg

  1. 1. “ Acid Base Imbalance” author Dr.Praveen Pawal Jr. medicine m.l.b .medical college jhansi.u.p Seminar Department of Medicine MLB Medical College, Jhansi
  2. 2. <ul><li>ACID BASE IMBALANCE </li></ul><ul><li>Acid base balance is important for the maintenance of normal cellular functions. Precise regulation of pH in a narrow range of 7.35 to 7.45 is essential. </li></ul><ul><li>pH is vital for – </li></ul><ul><li>normal cellular enzymatic reactions. </li></ul><ul><li>normal ionic concentration </li></ul><ul><li>Change in pH can cause cardiac arrhythmias. Extreme range of pH (i.e. <7.2 or >7.55) are potentially life threatening. </li></ul>
  3. 4. <ul><li>The concept of pH was first introduced by  Danish   chemist   Soren Peder Lauritz Sorensen  at the  Carlsberg Laboratory  in 1909. It is unknown what the exact definition of p is. Some references suggest the p stands for “ Power”, others refer to the German word “Potenz ” (meaning power in German), still others refer to “potential ”. Jens Norby published a paper in 2000 arguing that p is a constant and stands for “negative logarithm”, which has also been used in other works. H stands for Hydrogen. Sorensen suggested the notation &quot;PH&quot; for convenience, standing for &quot;power of hydrogen&quot;,using the logarithm of the concentration of hydrogen ions in solution, p[H] .  Although this definition has been superseded ,p[H] can be measured if an electrode is calibrated with solution of known hydrogen ion concentration. </li></ul>
  4. 5. Basic terminology pH – signifies free hydrogen ion concentration. pH is inversely related to H + ion concentration. Acid – a substance that can donate H + ion, i.e. lowers pH. Base – a substance that can accept H + ion, i.e. raises pH. Anion – an ion with negative charge. Cation – an ion with positive charge. Acidaemia – blood pH< 7.35 with increased H + concentration. Alkalaemia – blood pH>7.45 with decreased H + concentration. Acidosis – Abnormal process or disease which reduces pH due to increase in acid or decrease in alkali. Alkalosis – Abnormal process or disease which increases pH due to decrease in acid or increase in alkali.
  5. 6. <ul><li>Basic physiology of acid base regulation </li></ul><ul><li>The body maintains pH within a normal range inspite of dietary intake of acid and alkali and endogenous acid production. </li></ul><ul><li>Normally, when food is metabolized, two types of acids are added to ECF. </li></ul><ul><li>Volatile acid – </li></ul><ul><li>H 2 CO 3 – 22,000 mEq/day </li></ul><ul><li>Non volatile acid </li></ul><ul><li>Sulphuric acid </li></ul><ul><li>Phosphoric acid – 1 mEq/kg/day </li></ul>
  6. 7. Regulation of acid base The regulation of pH in a narrow range is the function of buffers, lung and kidney. The Henderson – Hasselbalch equation describes the correlation between metabolic and respiratory regulations, which maintains pH. Buffers – Buffers are chemical systems which either release or accept H + . So, buffers minimize change in pH induced by an acid or base load and provide immediate defense, but have least buffering power. e.g. – bicarbonate, bone bicarbonate, proteins, phosphate, Hb. Respiratory regulation – by excreting volatile acids, lungs regulate PaCO 2 . When amount of CO 2 increases in body , it will stimulate PaCO 2 sensitive chemoreceptors at central medulla, with resultant rise in rate and depth of breathing. pH = 6.1+log HCO 3 - PaCO 2 ×0.0301
  7. 8. This hyperventilation will maintain PaCO 2 at normal range. Respiratory regulation acts rapidly (in seconds to minutes) and has double buffering power as compared to chemical buffers. CO 2 + H 2 O  H 2 CO 3  H + + HCO 3 - HbH  H + + Hb HCO 3 - Tissue CO 2 Venous Blood Cl -
  8. 9. HCO 3 - O 2 Alveolar capillary barrier Cl - O 2 + HbH  HbO 2 + H + H + + HCO 3 -  H 2 o + CO 2 Lung
  9. 10. <ul><li>Renal regulation :- Role of kidney is to maintain plasma HCO 3 - and thus pH. It’s the most powerful buffering system, starts within hrs and takes 5-6 days for peak effect. </li></ul><ul><li>HCO 3 - regulation is done by -: </li></ul><ul><li>Reabsorption of filtered bicarbonate ion. </li></ul><ul><li>Production of new HCO­ 3 - ion by formation of titratable acid </li></ul><ul><li>Excretion of NH­ 4 + in urine. </li></ul>
  10. 11. Bicarbonate resorption Blood Kidney H + + HCO 3 - H 2 CO 3 CO 2 <ul><li>Proximal tubules </li></ul><ul><li>Collecting ducts </li></ul><ul><li>Distal tubules </li></ul>CO 2 + H 2 O  HCO 3 - + H + HCO 3 - Glutamine HCO 3 - NH 4 + HCO 3 - Ammonia excretion NH 4 + Cl - NH 4 Cl - CO 2 + H 2 O  HCO 3 - + H + HCO 3 - Titratable acid formation H + H 2 PO 4 -
  11. 12. <ul><li>Arterial Blood Gas Analysis </li></ul><ul><li>Arterial blood gas (AG) measurements are invaluable in assessing the adequacy of pulmonary gas exchange and the presence and severity of acid base disturbances. </li></ul><ul><li>Proper interpretation of PaO 2 , PaCO 2 and pH values require knowledge of the clinical state of the patient, the therapy given and other data like Hb concentration, cardiac output. </li></ul><ul><li>Sampling technique – of choice for routine analysis is direct radial artery puncture. </li></ul><ul><li>Perform modified Allen’s test. </li></ul><ul><li>Clean the site. </li></ul><ul><li>Use 21 guaze needle with syringe. </li></ul><ul><li>Flush syringe and needle with heparin. </li></ul><ul><li>Enter skin at 45° angle. </li></ul>
  12. 13. <ul><li>Obtain 2-4ml blood without aspiration. Avoid suction of syringe . </li></ul><ul><li>If sample contains any air bubble, tap it to the surface and push it out of the syringe. Air bubbles can lead to increase in PaO 2 and decrease in PaCO 2 . </li></ul><ul><li>Apply firm pressure at punctured site. </li></ul><ul><li>Note : </li></ul><ul><li>The determination of acid base status does not necessarily require sampling of arterial blood. The best reason to sample arterial blood is to determine the state of oxygenations. Venous blood is perfectly acceptable for acid base determination if oxygen is not in question. </li></ul><ul><li>The sum of PO 2 and PCO 2 should be less than 140mmHg if the patient is breathing room air. </li></ul><ul><li>ABG and serum electrolytes should be performed simultaneously for correct interpretation of acid base disorders. </li></ul>
  13. 17. Normal ABG Values -: Na + 135-145meq/lt K + 3.5-5.5meq/lt TCO 2 21-30meq/lt iCa 1.1-1.4mmol/lt HCT 47 + 7% (male) 42 + 5% (female) Hb 13.5-17.5 (male) 12-16 (female) At 37°C pH 7.35-7.45 PCO 2 40±5mmHg PO 2 95±5mmHg HCO 3 - 24±2 mEq/lt BE etc ±2 mEq/lt SPO 2 97 ۬ ±2%
  14. 18. <ul><li>Aids in establishing a diagnosis </li></ul><ul><li>Helps guide treatment plan </li></ul><ul><li>Aids in ventilator management </li></ul><ul><li>Improvement in acid/base management allows for optimal function of medications </li></ul><ul><li>Acid/base status may alter electrolyte levels critical to patient status/care </li></ul>
  15. 19. TCO 2 :- Total CO 2 content of plasma is the sum of the plasma concentration of HCO 3 - , dissolved CO 2 and H 2 CO 3 . The contribution of CO 2 and H 2 CO3 is small. Hence, total CO 2 in plasma and HCO 3 concentration are often used interchangeably. Base excess :- is derived from whole blood buffer base, defined as sum of concentration of buffer anions (HCO 3 - and Hb) in whole blood. BE is defined as difference between the observed and normal values for whole blood buffer base. It is used to overcome the limitation of plasma HCO 3 - as an index of acid base status.
  16. 20. <ul><li>In human physiology , base excess refers to the amount of acid required to return the blood pH of an individual to the reference interval pH (7.35 - 7.45) with the amount of carbon dioxide held at a standard value(ie pCO2-40mmHg). The value is usually reported in units of (mEq/L). The normal reference range is somewhere between -2 to +2. </li></ul><ul><li>Another definition for base excess is the amount of acid or base that must be added to a litre of blood (ECF) to return the pH to 7.4 at a pCO2 of 40 mmHg. </li></ul><ul><li>Base excess can be calculated by the Van Slyke equation. Base excess is a positive figure, indicating metabolic alkalosis, while base deficit is a negative figure and indicative of acidosis (normal range- ( -2 to +2). </li></ul>
  17. 21. B ase excess = 0.93 ( HCO 3 - 24.4 + 14.8(pH - 7.4)) Alternatively expressed: Base excess = 0.93 HCO 3 + 13.77 pH - 124.58 Van Slyke equation--
  18. 22. SO 2 :- Percent of O 2 attached to Hb PaO 2 :- Pressure with which O 2 is dissolved in blood. 90% 60 mmHg 10% PaO 2 SO 2 Oxygen Dissociation Curve – Sigmoid shaped curve
  19. 24. <ul><li>Hypoxia ;refers to any state in which tissue receive inadequate supply of o2 to support normal aerobic metabolism i.e., Hypoxaemia, Ischaemia </li></ul><ul><li>Hypoxaemia ; refers to any state in which o2 content of arterial blood is reduced that is impaired oxegenation, low haemoglobin . </li></ul><ul><li>Impaired oxegenation :-Refers to hypoxaemia resulting from reduced transfer of o2 from lungs to bloodstream . </li></ul>
  20. 26. Assessing severity of type 1 respiratory impairment Mild Moderate Severe Pao2(kPa) 8-10.6 5.3-7.9 <5.3 Pao2 60-79 40-59 <40 Sao2 90-94 75-89 <75 Other markers of severe impairment <ul><li>High Fio2 requirement to maintain adequate Pao2 </li></ul><ul><li>Lactic acidosis (indicating tissue hypoxia) </li></ul><ul><li>Organ dysfunction (drowsiness, confusion,renal failure, haemodynamic collapse, coma) </li></ul>
  21. 27. Common causes of type 2 respiratory impairment Chronic obstructive pulmonary disease Opiate /benzodiazepine toxicity Exhaustion Inhaled forein body Flail chest injury Neuromuscular disorders Kyphoscoliosis Obstructive sleep apnoea The ABG in different pattern of type 2 impairment Paco2 HCo3 Ph Acute ↑ -> ↓ Chronic ↑ ↑ -> Acute on chronic ↑ ↑ ↓
  22. 28. A-a gradient The A-a gradient is the difference between the po 2 in alveoli (PAo 2 ) and the Po 2 in aterial blood (Pao 2 ). Pao 2 is measured on ABG but PAo 2 has to be calculated using the alveolar gas equation A-a gradient = PAo 2 - Pao 2 It is normally less than 2.6 kpa (20 mmHg), although it increases with age and Fio2 .This means that : 1.the normal range for Pao2 falls with age 2.the A-a gradient is most accurate when performed on room air. Simplefied alveolar gas equation PAo2 (kpa) = (Fio2 x 93.8)-(Paco2 x 1.2) Or PAo2 (mmHg) = (Fio2 x 713)-(Paco2 x 1.2) Assumes the patient is at sea level and has a body temperature of 37°
  23. 29. <ul><li>BASICS OF ACID BASE DISORDER AND COMPENSATION </li></ul><ul><li>Four primary acid base disorder are defined :- </li></ul><ul><li>If initial disturbance affects HCO 3 - </li></ul><ul><li>Metabolic acidosis HCO 3 -  </li></ul><ul><li>Metabolic alkalosis HCO 3 -  </li></ul><ul><li>If PaCO 2 affected first </li></ul><ul><li>Respiratory acidosis (  PaCO 2 ) </li></ul><ul><li>Respiratory alkalosis (  PaCO 2 ) </li></ul>
  24. 30. Compensation – The body’s response to neutralize the effect of the initial insult on pH homeostasis is called compensation. pH Primary change Secondary change Metabolic acidosis Low HCO 3  PaCO 2  Metabolic alkalosis High HCO 3  PaCO 2  Respiratory acidosis Low PaCO 2  HCO 3  Respiratory alkalosis High PaCO 2  HCO 3 
  25. 31. Rule of same direction :- In simple acid base disorders, HCO 3 and PaCO 2 compensatory change are in the same direction as the primary changes.  HCO 3 leads to  PaCO 2  HCO 3 leads to  PaCO 2 This will bring pH to near normal although not to normal. If these changes are in opposite direction or the actual changes are not equal to expected, it suggests mixed disorder.
  26. 32. 2-Metabolic alkalosis (  HCO 3 )- Rise in PaCO 2 =0.75x Rise in HCO 3 3-Respiratory acidosis   PaCO 2 )-- Acute - Rise in HCO 3 =0.1x Rise in PaCO 2 Chronic - Rise in HCO 3 = 0.4x Rise in PaCO 2 4-Respiratory alkalosis   PaCO 2 )--- Acute - Fall in HCO 3 =0.2x Fall in PaCO 2 Chronic - Fall in HCO 3 = 0.4x Fall in PaCO 2 1-Metabolic acidosis (  HCO 3 )– Expected PaCO 2 = (1.5 × HCO 3 - ) +8 OR PaCO 2 = HCO 3 - + 15
  27. 33. By calculating compensation, we can differentiate between simple and mixed disorder. If expected change = actual change, disorder is simple If actual change is more or less than predicted, disorder is mixed. Mixed disorder :- defined as independent coexistence of more than one primary acid base disorder. Most common is mixed metabolic acidosis and respiratory acidosis.
  28. 34. Common mixed acid base disorders Disorders Common causes <ul><li>Metabolic acidosis and Respiratory acidosis </li></ul><ul><li>(low pH,  HCO 3 ,  PaCO 2 ) </li></ul><ul><ul><li>Cardiac arrest (hypoventilation + lactic acidosis) </li></ul></ul><ul><ul><li>Shock with respiratory failure </li></ul></ul><ul><li>Metabolic acidosis and Respiratory alkalosis </li></ul><ul><li>(N.pH,  HCO 3 ,  PaCO 2 ) </li></ul><ul><ul><ul><li>Salicylate intoxication c.Gram negative sepsis </li></ul></ul></ul><ul><ul><ul><li>Liver failure d.malarial pyrexia </li></ul></ul></ul><ul><ul><ul><li>e. Diabetic ketoacidosis with respiratory disease </li></ul></ul></ul><ul><li>Metabolic alkalosis and Respiratory acidosis </li></ul><ul><li>(N.pH,  HCO 3 ,  PaCO 2 ) </li></ul><ul><li>COPD with diuretics </li></ul><ul><li>Metabolic alkalosis with severe hypokalemia and respiratory weakness leads to hypoventilation </li></ul><ul><li>Metabolic alkalosis and Respiratory alkalosis </li></ul><ul><li>(  pH,  HCO 3 ,  PaCO 2 ) </li></ul><ul><li>Liver failure with vomiting </li></ul><ul><li>Patient on ventilator with continuous nasogastric aspiration </li></ul><ul><li>Metabolic acidosis and metabolic alkalosis </li></ul><ul><li>(near N.pH and HCO 3 ) </li></ul><ul><li>Diabetic ketoacidosis with vomiting </li></ul><ul><li>Vomiting with severe volume depletion causing lactic acidosis </li></ul><ul><li>Respiratory acidosis </li></ul><ul><li>Respiratory alkalosis </li></ul>Do not co-exist
  29. 35. <ul><li>Evaluation and investigation of acid base disorder </li></ul><ul><li>History and clinical examination. </li></ul><ul><li>Primary investigation – S.Na + , K + , Cl - , HCO 3 - , anion gap, CBC, urinary electrolytes, blood sugar, renal function test etc. </li></ul><ul><li>ABG is mandatory for diagnosis of acid base disorder. </li></ul><ul><li>Anion gap :- The charge difference between unmeasured anion and cation is termed the anion gap. </li></ul><ul><li>Unmeasured anions – anionic protein, phosphate, sulphate and organic acids. </li></ul><ul><li>Unmeasured cations – Ca ++ , Mg ++ , K + </li></ul><ul><li>AG = (Na+ K + ) – (HCO 3 - + Cl) </li></ul><ul><li>Normally, AG = 12±2 mEq/lt </li></ul><ul><li>Albumin normally compromises most of the anion gap. </li></ul><ul><li>1gm/dl  in S.alb – 2mEq/lt  in AG </li></ul>
  30. 36. <ul><li>Uses </li></ul><ul><li>Useful for etiological diagnosis of metabolic acidosis </li></ul><ul><li>Diagnosis of mixed disorder </li></ul><ul><li>Step by step analysis </li></ul><ul><li>Is there an acid base disorder – look for PaCO 2 and HCO 3 - </li></ul><ul><ul><li>If normal – No acid base disorder, or </li></ul></ul><ul><li>Mixed acid base disorder ( specially in critically ill patients ) </li></ul><ul><ul><li>If abnormal – Acid base disorder present </li></ul></ul><ul><li>Look at pH </li></ul><ul><li>pH < 7.35 – acidosis </li></ul><ul><li>pH >7.45 – alkalosis </li></ul>
  31. 37. <ul><li>Whether its primary acid base disorder </li></ul><ul><li>If pH < 7.35 Metabolic acidosis  HCO 3 </li></ul><ul><li>Respiratory acidosis  PaCO 2 </li></ul><ul><li>If pH > 7.45 Metabolic alkalosis  HCO 3 </li></ul><ul><li>Respiratory alkalosis  PaCO 2 </li></ul><ul><li>Calculate the expected compensation- If the actual value matches with the expected compensation, it confirms diagnosis of primary disorder. </li></ul><ul><li>How to determine the presence of mixed acid base disorder--- </li></ul><ul><li>Check direction of change- In simple acid base disorder, HCO 3 and PaCO 2 change from normal in same direction. If changes are in opposite direction, it suggests mixed disorder. </li></ul>
  32. 38. <ul><li>Compare expected compensation with actual value - if actual value is either more or less as compared to the calculated expected compensation, it suggest mixed disorder. </li></ul><ul><li>Check anion gap </li></ul><ul><li>Compare fall in HCO 3 with increase in plasma anion gap </li></ul><ul><li>Rise in AG = Fall in HCO 3 - , it shows high AG metabolic acidosis </li></ul><ul><li>If  in AG exceeds fall in HCO 3 , it suggests coexisting metabolic alkalosis. </li></ul><ul><li>If  in AG is less than fall in HCO 3 , it suggests loss of HCO 3 - (diarrhea) causing non AG metabolic acidosis. </li></ul><ul><li>Clinical correlation and establish the diagnosis </li></ul>
  33. 40. <ul><li>Case studies </li></ul>
  34. 41. <ul><li>20 yrs,male Anurag working in printing press brought in emergency department at 4 PM on 1 st July 2009 by his family members with history of consumption of dye used in printing press, before 4 hours after quarrel with his father. </li></ul><ul><li>At the time of admission pt was unconscious, his vitals were as follows - </li></ul><ul><li>BP-110/70 mm of Hg </li></ul><ul><li>PR-80/min </li></ul><ul><li>Temp-Normal </li></ul><ul><li>RR-10/min Spo2-67% </li></ul><ul><li>cyanosis-Present </li></ul><ul><li>Pupils-NSNR </li></ul><ul><li>Typical smell of aniline dye </li></ul>
  35. 43. <ul><li>On systemic examination – </li></ul><ul><li>Chest –B/L clear </li></ul><ul><li>All other systemic examination were WNL. </li></ul><ul><li>Management – </li></ul><ul><li>ABG was done along with routine blood investigation </li></ul>
  36. 44. ABG Ph 6.95 PCo 2 23.9mm Hg P0 2 45mmHg Bicarb 5.3 mmol/l BE -27 S0 2 55% K 2.2 mmol/l Na 140 mmol/l Cl 118 mmol/l iCa+ 0.87 Hb 11.9 gm /dl
  37. 45. <ul><li>Since PH=6.95 so acidosis. </li></ul><ul><li>HCO 3 =5.3, so primary disorder is metabolic acidosis </li></ul><ul><li>whether it is compensated or not? </li></ul><ul><li>Expected fall in PCO 2 </li></ul><ul><li>=(1.5 x HCO 3 )+8 </li></ul><ul><li> = (1.5 x 5.3) +8 </li></ul><ul><li>= 15.95 </li></ul><ul><li>But actual value of Pco 2 = 23.9 which is more then expected. </li></ul><ul><li>So it mixed disorder i.e. metabolic acidosis with Respiratory acidosis with hypokalemia, and as Po 2 is 45 mmHg and so 2 is 55% so there is hypoxemia because of methemoglobinemia and repiratory depression due to hypokalemia leading to respiratory acidosis because of hypoventilation. </li></ul>
  38. 46. <ul><li>Anion Gap = (Na + + K + )-(Hco3 + Cl-) </li></ul><ul><li>= (140+2.2) –(5.3+118) </li></ul><ul><li>= 142.2-122.3 </li></ul><ul><li>= 19.9( Normal Value 10-12 mmol) </li></ul><ul><li>i.e. it is High anion gap metabolic acidosis . </li></ul><ul><li>To correct acid base disorder i/v soda bicarb along with supplemental K + infusion done. </li></ul><ul><li>Amount of sodabicarb to be given was- </li></ul><ul><li>=(Desired HCo 3 - Actual Hco3) X 0.5X BW </li></ul><ul><li>=(15-5.3)x0.5x60 </li></ul><ul><li>= 9.7x30=291 meq(14 amp of HCo 3 ) </li></ul><ul><li> </li></ul>
  39. 47. <ul><li>1 ampule of sodabicarb contains 22 meq. </li></ul><ul><li>So total 14 ampules will be given, out which half amount i.e.7ampules given with in first 1-2 hours & next 7 during remaining 24 hours. </li></ul><ul><li>To correct hypoxia,100% o 2 inhalation along with oral methylene blue in doses of 200 mg in divided doses to reverse methemoglobinemia was given. </li></ul>
  40. 48. <ul><li>Amount of K + to be given is- </li></ul><ul><li>Since our pts K is 2.2mEq so defficiency is approx 450-600mEq. Maximum dose which can be given in 24 hrs should not be more then 240meq & the infusion rate should not be >20meq/hr. </li></ul><ul><li>1amp of KCl contains 20 meq of K. </li></ul><ul><li>KCl should be mixed with isotonic saline.Dont mix this with D-5% as diluent. </li></ul>
  41. 49. <ul><li>Kamlesh 40 yrs male admitted in emergency deptt. On 06 Sep. 09 at 10 AM as acute onset ascending LMN type of quadriplegla with difficulty in respiration without bladder and bowel involvement and without any sensory impairment .Pt had history of high grade fever with sore throat 8 days back for 2 days. </li></ul>
  42. 51. <ul><li>Pt diagnosed as a case of GB syndrome with respiratory muscles paralysis. </li></ul><ul><li>On examination at the time of presentation - </li></ul><ul><li>PR -90/min </li></ul><ul><li>BP -140/90 mm Hg </li></ul><ul><li>Temp –Normal </li></ul><ul><li>RR-8/min, accessory muscles of respiration are working . </li></ul><ul><li>SPO 2 -74% </li></ul><ul><li>Pt immediately intubated and put on ventilator on SIMV+PSVmode.Pt ABG was done within half hour which was- </li></ul>
  43. 53. <ul><li>pH-7.328 i.e. acidosis </li></ul><ul><li>pCO2 =48.6 i.e. respiratory acidosis (primary disorder due to CO 2 retention because of respiratory muscle paralysis ie TYPE II respiratory failure-acute). </li></ul><ul><li>Now wheather it is compensated or not ? </li></ul><ul><li>For acute respiratory acidosis rise in HCO 3 - should be </li></ul><ul><li>= 0.1 X Rise in pCO 2 </li></ul><ul><li>= 0.1X (48.6-40) </li></ul><ul><li>= 0.1 X 8.6 </li></ul><ul><li> = 0.86 </li></ul>
  44. 54. <ul><li>So expected value of HCO 3 - should be – </li></ul><ul><li>HCO 3 - = 24+0.86 </li></ul><ul><li>= 24.86 </li></ul><ul><li>= 25 </li></ul><ul><li>And actual value of HCO 3 - is 25 which is equal to expected valve. So it is compensated respiratory acidosis because of type II respiratory failure. </li></ul>
  45. 55. Case 3 Date :02/04/09 Patient Name : Smt Kranti 26yrs Female Case of type 1 DM diagnosed 4 months back had discontinued medication from 1 month. Came here with C/C - 1-Fever x 2 day 2-Pain in knee joint x 2 days 3-Breathlessness x 2 day PR- 110/min BP -100/ 70mm Hg RR 30/min Dehydration++ Investigations--- RBS >500 mg Ketone: large Sugar : ++++ S.creat. :1.10 mg/dl TLC : 24,100/cmm
  46. 57. ABG 02/04/09 Ph 6.99 PCo 2 10.5 mmHg P0 2 111 mmHg BE -29 mmol/L HCo3 2.6 Tco2 45 SO2 95 Na+ 138 mmol/L K+ 4.2 mmol/L iCa+ 1.06 mmol/L Hb 12.6 g/dl
  47. 58. <ul><li>Since PH=6.99 so acidosis. </li></ul><ul><li>HCO 3 =2.6, so primary disorder is metabolic acidosis </li></ul><ul><li>whether it is compensated or not? </li></ul><ul><li>Expected fall in PCO 2 </li></ul><ul><li>=(1.5 x HCO 3 )+8 </li></ul><ul><li> = (1.5 x 2.6) +8 </li></ul><ul><li>= 11.9 </li></ul><ul><li>But actual value of Pco 2 = 10.5 which is less then expected. </li></ul><ul><li>So it mixed disorder i.e. metabolic acidosis with Respiratory alkalosis. </li></ul>
  48. 59. Management DKA with severe metabolic Acidosis with respiratory alkalosis. 1- IV Antibiotics 2- HCO3 Deficity Calculated --- =O.5 X (BW) (actul HCO 3 - DesiredHCO 3 ) =0.5 x 40x 12.3 = 247 Meq/L (11 amp of sodabicarb) out of which half is given with in 2 hr & rest to be given over 24 hrs IV. 3- Inj insulin R accordingly to RBS. 4- IVF : NS ISO -M
  49. 60. 03/04/09 Ph 7.462 PCo 2 30.1 mmHg P0 2 107mmHg BE -2 mmol/L HCo3 21.6 Tco2 15 So2 96 Na+ 138.6 mmol/L K+ <2.0 mmol/L iCa+ 1.0 mmol/L Hb 12.1 g/dl
  50. 61. Next day ABG was repeated pt had mild(metabolic Acidosis with Respiratory alkalosis) with hypokalemia may because of i/v NAHCO3 & insulin both of which causes intracellular shift of potassium .Hypokalemia was corrected. Pt improved.
  51. 62. Case 4 Pt Pyarelal 20 yrs old admitted here on 31 st August 2009 with complain of snake bite in night with features of respiratory muscles paralysis. Pt was immediately intubated and put on mechanical ventilation. After resumption of spontaneous breathing pts ABG was done on next day at 3:52 PM to decide wheather to wean off from ventilator or not. Pt’s ABG was -----
  52. 65. Ans Pts pH is normal i.e.7.42 PCO2 is normal i.e. 39.9 HCO3 is within normal range i.e.26 PO2 is 75 mm Hg It means pt’s ABG is normal except decrease PO2 .So pt can be weaned of from ventilator after assessing the clinical condition and supplemental O2 should be given by mask On assessing it was seen that pt was properly breathing with full effort and depth, RR is 16/min, pt was weaned off from ventilator in the evening and put on T-Tube breathing with supplemental oxygen, pt survived.
  53. 66. Case 5 Pt Ramchandra 29 yrs/male admitted here with complain of 10-12 loose motions per day with passage of blood along with fever for 3 days, for 1 day he also c/o decreased amount of urine. For all these he was admitted here and managed on the lines of acute gastroenteritis with ARF. On next day of admission he develops breathlessness with deterioration in his condition for which ABG was done which shows-
  54. 69. Analysis of ABG Pt is pH is 7.46 ie alkalosis, pCO2 is 19. So it is Respiratory alkalosis. For acute Resp. alkalosis--- Fall in HCO3- =0.2 X Fall in PaCO2 = 0.2 x (40-19) =0.2 X 21=4.2 so expected HCO3 = 24-4.2 = 19.8 but actual HCO3=13.5 which is less then the expected. So it is mixed disorder with metabolic acidosis due to hypoperfusion , renal failure, lactic acidosis due to sepsis and loss of HCO3 during diarrhea with Resp. alkalosis due to hyperventilation because of sepsis.
  55. 70. Case 6 58 years old male Gyasi admitted to Hospital with C/C -- 1-Fever chills and rigor x 8 days 2-Altered sensorium x 4 hrs 3-Breathlessnes x 4 hrs 4-Decreased urine output O/E : Pt unconscious PR- 90/min BP -70 systolic RR- 28 /min INVESTIGATION: Sr creatnine: 13.50 mg /dl Hb:4.80 g/dl TLC :27,200/cmm P-90 L-03 QBC-Negative
  56. 72. ABG Na + 139 K+ 5.3 Tco 2 0.65 Hb 5.0 PH 6.798 Pco 2 10 Po 2 120 HCO 3 1.5 BE -30 SO 2 93%
  57. 73. <ul><li>Since pH=6.798 so acidosis. </li></ul><ul><li>HCO 3 =1.5, so primary disorder is metabolic acidosis </li></ul><ul><li>whether it is compensated or not? </li></ul><ul><li>Expected fall in PCO 2 </li></ul><ul><li>=(1.5 x HCO 3 )+8 </li></ul><ul><li> = (1.5 x 1.5) +8 </li></ul><ul><li>= 10.25 </li></ul><ul><li>actual value of PCO 2 = 10.25 which is equal to expected. </li></ul><ul><li>So it is severe metabolic acidosis with hyperkalemia .Pt has hyperkalemia ,pH <7.1 & S.bicarbonate is <10 so NAHCO3 is given i/v. </li></ul><ul><li>, </li></ul>
  58. 74. Amount of sodabicarb to be given ---- =(Desired HCO 3 - Actual HCO3) X 0.5X BW =(10-1.5) x 0.5 x 50 =212 (about 12 amp of SBC to be given ,out of which half of dose should be given in 1 st hr & rest over next 24 hrs ). Management --- BT II ⨀ Antibiotic Antimalarial Antihyperkalemic Peritoneal Dialysis was planned Patient expired before intervention was done.
  59. 75. Case 7 Name : Vandana 23 yrs ,Female k/c/ o pul koch’s four times defaulter(CAT II) Came her with C/C --- Breathlessness at rest O/E : Pt nutrition was poor and malnourished PR- 100/min BP- 100/70 mmHg Chest : B/L crepts X-ray : Rt side pnemothorax localised with extensive b/l infiltration. TLC -8900 P-83 L-14 E-2 Sr.crt : 1.0mg/dl Sr .billirubin : 0.64mg/dl SPO2 : 66 %
  60. 76. ABG Na+ 134 K+ 3.5 Tco 2 27 ica 0.86 HCt 37 Hb 12.6 Ph 7.516 Pco 2 31.8 Po 2 36 Hco 3 25.2 BE 3 m mol/L So 2 65 %
  61. 77. <ul><li>Since Ph is 7.516, so alkalosis. </li></ul><ul><li>pCO2 is 31.8,so it is respiratory alkalosis. </li></ul><ul><li>Now expected fall in HCO3 should be---- </li></ul><ul><li>= 0.4 x Fall in Pco2 </li></ul><ul><li>= 0.4x8.2=3.3 </li></ul><ul><li>So expected HCO3 should be=24-3.3=21.7 </li></ul><ul><li>But actual value of HCO3 is—25.2 </li></ul><ul><li>So it mixed disorder ie respiratory alkalosis (due to Type 1 respiratory failure) with metabolic alkalosis ( may be due to chronic use of steroids). </li></ul>
  62. 78. Management ---- High flow oxygen Therapy IV Antibiotics ATT as advised by DOTS.
  63. 79. Case 8 Biharilal 60 yrs male. Admitted as case of Pul koch’s with Syst HTN was taking ATT & Amlong H. C/C : 1- low grade fever 2- ↓ Appetite 3- Lethargy O/E: PR-92/min regular BP :150/90 mm Hg Chest :: B/L crepts ++ Dehydration ++
  64. 82. pH: 7.449 So alkalosis HCO3 is 26.8 Primary disorder is metabolic Alkalosis. So expected rise in Paco2= 0.75X Rise in HCO 3 = 0.75X2.8 = 2.1 So expected paco2= 40+2.1 = 42.1 so it is mixed disorder ie metabolic alk alosis with ECF volume depletion due to thiazide diuretics and Respiratory alkalosis due to hyperventilation with hyponatrimia with hypokalemia.
  65. 83. <ul><li>As our pts S.Na is 110 meq/l ie severe hyponatremia. </li></ul><ul><li>First rule out the causes of pseudohyponatremia. Then we calculate serum osmolality,which is hypoosmolar in our pt. </li></ul><ul><li>Now we assess renal status which is normal in our pt ,after this we assess volume status of our pt which is depleted. </li></ul><ul><li>Now urine Na should be assesed.In our case it should be more then 20 to lebel it as diuretic induced hyponatremia. </li></ul>
  66. 84. <ul><li>First we stop the diuretic. </li></ul><ul><li>Now we supplement fluid & salt which can be done with i/v isotonic saline 0.9% at rate appropriate for the estimated volume depletion. </li></ul><ul><li>The targeted rate of Na correction should not be greater then 0.5 to 1 meq/l/hr & it should not exceed 8 meq/l on any day of treatment. </li></ul><ul><li>Na requirement=(Desired Na-Actual Na)x0.5xBW(kg) </li></ul><ul><li>0.9%NaCl per liter = 154 meq of Na </li></ul><ul><li>3%NaCl per liter = 514 meq of Na </li></ul>
  67. 85. <ul><li>Date : 06/08/09 </li></ul><ul><li>Name : Gori Bai Age: 50 yrs Female </li></ul><ul><li>MRDNO: 14592 </li></ul><ul><li>C/C: Loose motion 15- 18 times x4 days </li></ul><ul><li>B.P-80/60 mmHg </li></ul><ul><li>Investigations: </li></ul><ul><li>Hb-12.3 </li></ul><ul><li>TLC 24100 cmm P- 78 L -18 </li></ul><ul><li>Plt- 1.65 </li></ul><ul><li>S.Billirubin- 0.77 mg/dl </li></ul><ul><li>S.Creatinine -2.29 mg/dl </li></ul><ul><li>Na + 124.8 mmol/l </li></ul><ul><li>K + 2.78 mmol/l </li></ul>
  68. 86. ABG 07/08/09 PH 7.27 PCo 2 17.9 P0 2 101 BECF -20 HCo 3 6.6 Tco 2 7 So 2 97 Na+ 124 K+ 2.78 iCa+ 0.25 Cl- 108
  69. 87. <ul><li>Since pH is 7.27 so it is acidosis. </li></ul><ul><li>HCO 3 is 6.6, so it is metabolic acidosis. </li></ul><ul><li>Now whether compensated or not? </li></ul><ul><li>Expected PCO 2 =(1.5 X HCO3-)+8 </li></ul><ul><li>=(1.5 X 6.6) +8 </li></ul><ul><li>= 9.9 +8 </li></ul><ul><li>= 17.9 </li></ul><ul><li>=18 </li></ul><ul><li>Actual PCO 2 =17.9 </li></ul><ul><li>So it is compensated metabolic acidosis </li></ul>
  70. 88. <ul><li>Anion Gap = (Na + + K + )-(HCO3 + Cl-) </li></ul><ul><li>= (124+2.78) –(6.6+108) </li></ul><ul><li>= 126.78-114.6 </li></ul><ul><li>= 12( Normal Value 10-12 mmol) </li></ul><ul><li>i.e. it is Normal anion gap metabolic acidosis . </li></ul><ul><li>To correct acid base disorder i/v Soda bicarb is given. </li></ul><ul><li>Amount of sodabicarb to be given was- </li></ul><ul><li>=(Desired HCo 3 - Actual Hco3) X 0.5X BW </li></ul><ul><li>=(15-6.6)x0.5x60 </li></ul><ul><li>= 8.4x30=252 meq(ie 12 ampules of Sodabicarb over 24 hrs). </li></ul>
  71. 89. Case10 History A 25 year old man, with no significant past medical history. Presents to the emergency department with a 2-day history of fever, productive cough and worsening breathlessness. Examination   He is hot and flushed with a temperature of 39.3ºC. He does not appear distressed but is using accessory muscles of respiration. There is diminished chest expansion on the left with dullness to percussion, bronchial breathing and coarse crakles in the left lower zone posteriorly.   Pulse 104 beats/min Respiratory rate 28 breaths/min Blood pressure 118/70 mmHg SaO 2 89%
  72. 90. H+ 31.8 nmol/L Ph 7.50 PCo 2 3.74 kPa 28.1 mmHg P0 2 7.68 kPa 57.8 mmhg Bicarb 23.9 mmol/L BE -0.5 mmol/L SP0 2 88.7% Lactate 1.2 K 3.7 mmol/L Na 138 mmol/L Cl 99 mmol/L iCa+ 1.2 mmol/L Hb 15 g/dl
  73. 91. Answer:- This patient has moderate type 1 respiratory impairment. Hyperventilation is an appropriate response to the hypoxaemia and sensation of dyspnoea and has resulted in a mild alkalaemia (remember that metabolic compensation does not occur in response to acute respiratory acid-base disturbance). The correct management for his condition is supplemental oxygen to correct the hypoxaemia and appropriate antibiotics to treat the infection. In a patient such as this, with moderate hypoxaemia and no ventilatory impairment, monitoring by pulse oximetry is more appropriate than repeated than repeated ABG sampling. Indications for further ABG analysis would include signs of exhaustion or hypercapnia or a further significant decline in Sao 2 .
  74. 92. <ul><li>Metabolic acidosis </li></ul><ul><li>Is characterized by fall in plasma HCO 3 , fall in pH (<7.35). PaCO 2 is reduced secondarily by hyperventilation, which minimizes the fall in pH. </li></ul><ul><li> HCO 3 - with acidemia. </li></ul><ul><li>Classified into high anion gap and normal anion gap acidosis. </li></ul>
  75. 93. <ul><li>Causes of high anion gap metabolic acidosis :- </li></ul><ul><li>Lactic acidosis </li></ul><ul><li>Ketoacidosis - Diabetic </li></ul><ul><li>Alcoholic </li></ul><ul><li>Starvation </li></ul><ul><li>Toxins - Propylene glycol </li></ul><ul><li>Ethylene glycol </li></ul><ul><li>Methanol </li></ul><ul><li>Pyroglutamic acid </li></ul><ul><li>Slicylates </li></ul><ul><li>Renal failure – Acute and chronic </li></ul><ul><li>Causes of normal anion gap acidosis :- </li></ul><ul><li>Diarrhoea   CA inhibitors </li></ul><ul><li>Ureterosigmoidostomy  Proximal RTA </li></ul><ul><li>Distal RTA  NH 4 Cl infusion </li></ul>
  76. 94. <ul><li>Clinical features – </li></ul><ul><li>A. Manifestation of underlying disorder </li></ul><ul><li>B. Manifestation of metabolic acidosis </li></ul><ul><li>Pulmonary – Kussmaul’s breathing </li></ul><ul><li>CVS – Cardiac arrhthmias,  response to inotropes, secondary hypotension (particularly when pH <7.2) </li></ul><ul><li>CNS – Headache, confusion, lethargy, dizziness, coma </li></ul><ul><li>Others – Anorexia, nausea, vomiting, muscular weakness, rickets in children and osteomalacia in adults. </li></ul><ul><li>Treatment </li></ul><ul><li>Treatment of underlying disorder. It is most important and may be the only required treatment for mild to moderate acidosis. </li></ul><ul><li>Alkali therapy – reserved for selected patients. </li></ul><ul><li>Correct volume and electrolyte deficits </li></ul>
  77. 95. <ul><li>Indications for alkali therapy </li></ul><ul><li>When blood pH <7.15-7.2. Such a severe acidosis is life threatening. </li></ul><ul><li>When HCO 3 falls below 10mEq/lt. Low HCO 3 needs prompt treatment because - </li></ul><ul><ul><li>Small additional fall in HCO 3 can cause a large fatal drop in pH. </li></ul></ul><ul><ul><li>Respiratory compensation requires heavy muscular work. Such compensatory hyperventilation for prolonged period can cause fatigue of respiratory muscles, and the patient may develop superimposed respiratory acidosis. </li></ul></ul><ul><li>Treatment of hyperkalemia with metabolic acidosis. </li></ul><ul><li>Bicarbonate is mainly required in normal AG acidosis but is controversial in increased AG acidosis. </li></ul>
  78. 96. <ul><li>Goal of treatment </li></ul><ul><li>The aim of treatment is to return blood pH to a safer level of about 7.2. </li></ul><ul><li>Bicarbonate must be increased to 10 mEq/lt. </li></ul><ul><li>Amount of HCO 3 required = </li></ul><ul><li>(Desired HCO 3 – Actual HCO 3 ) × 0.5 × Body weight (in kg) </li></ul><ul><li>Except in cases of extreme acidaemia, NaHCO 3 should be administered as an infusion over a period of several minutes to few hrs. </li></ul><ul><li>i.e. 50-100mEq of NaHCO 3 over 30-45min during initial 1-2hr of therapy. </li></ul>
  79. 97. <ul><li>Precaution during NaHCO 3 administration </li></ul><ul><li>NaHCO 3 is highly irritant, so establish proper large IV line. </li></ul><ul><li>Avoid IV bolus. </li></ul><ul><li>Correct hypokalemia as intracellular K + shifting can cause life threatening hypokalemia. </li></ul><ul><li>NaHCO 3 should be given with caution in circulatory overload. </li></ul><ul><li>Avoid mixing of calcium with NaHCO 3 , to avoid precipitation </li></ul><ul><li>Avoid mixing of NaHCO 3 with inotropes. </li></ul>
  80. 98. <ul><li>Disadvantage and risk of NaHCO 3 therapy </li></ul><ul><li>Hypernatremia and volume overload, specially in CHF and renal failure patients. </li></ul><ul><li>CNS acidosis and hypercapnia. </li></ul><ul><li>Hypokalemia and hypocalcemia. </li></ul><ul><li>Overshoot or rebound alkalosis in organic acidosis- due to conversion of accumulated organic anions into bicarbonate. </li></ul><ul><li>Stimulation of phosphofructokinase activity, enhances lactate production and worsens acidosis. </li></ul>
  81. 99. METABOLIC ACIDOSIS IN SPECIFIC SITUATION [ I ] Increased Anion Gap Acidosis 1. Lactic acidosis It is the most serious and most common cause of metabolic acidosis in hospitalized critically ill patients. The most common cause of lactic acidosis is shock (cardiogenic or septic) Type A - Characterized by impaired tissue oxygenation. Type B - No hypoxia but mitochondrial respiration is impaired.
  82. 100. Causes of lactic acidosis Diagnosis – Diagnose lactic acidosis in increased AG acidosis, by exclusion of ketoacidosis, intoxication, renal failure. Serum lactate levels confirm the diagnosis. Normal S. lactate level – 1mEq/lt Lactic acidosis – 4-5mEq/lt Commonly goes upto - 10-30mEq/lt. Type A Type B Shock (Cardiogenic or septic) Respiratory failure Carbon monoxide or Cyanide poisoning Severe anaemia Diabetes mellitus Hepatic failure Severe infection Toxins – Ethanol, Methanol Drugs - Biguanides
  83. 101. Treatment Goal of therapy is adequate tissue oxygenation and treatment of the underlying cause. Tissue oxygenation can be improved by high inspired oxygen fraction, ventilator support, repletion of ECF volume, after load reducing agents and inotropic support by dopamine and dobutamine. Avoid vasoconstricting drugs like noradrenaline, as they can worsen tissue hypoxia. Administration of NaHCO 3 is started late (pH <7.1) and discontinued early. Early bicarbonate hemodialysis is effective.
  84. 102. 2 . Diabetic ketoacidosis Due to overproduction of acetoacetic acid and  -hydroxybutyric acid due to relative or absolute insulin deficiency. Cornerstone of treatment is insulin administration, with replacement of water, Na + and K + . Alkali should not be administered routinely as insulin and supportive therapy regenerate bicarbonate from resolution of retained ketone bodies. Bicarbonate is indicated in patients where pH<7.1, the goal of therapy is to raise pH to relatively safe level of 7.2. HCO 3 is also indicated in severe hyperkalemia.
  85. 103. 3. Alcoholic ketoacidosis It occurs after abrupt discontinuation of alcohol consumption and is usually due to vomiting, prolonged starvation and volume depletion. Correction of hypoglycemia with dextrose infusion will stimulate insulin secretion and inhibit glucagon secretion and thereby promote regeneration of bicarbonate from metabolism of retained ketone bodies. Correction of hypovolemia will prevent ketoacidosis. Supplement thiamine with glucose to avoid development of Wernicke’s encephalopathy.
  86. 104. <ul><li>4. Salicylate (Aspirin) poisoning </li></ul><ul><li>It is characterized by respiratory alkalosis or mixed metabolic acidosis with respiratory alkalosis. Respiratory alkalosis is caused by direct stimulation of respiratory center by salicylates whereas accumulation of lactic and keto acids cause metabolic acidosis. </li></ul><ul><li>Treatment – </li></ul><ul><li>Gastric lavage </li></ul><ul><li>Correction of hypovolemia by saline </li></ul><ul><li>Forced alkaline diuresis </li></ul><ul><li>Increase in pH converts salicylates to more impermeable salicylic acid and thus prevents CNS damage. </li></ul>
  87. 105. Thus, unless blood is already alkalinzed by respiratory alkalosis, give NaHCO3 infusion – 88mEq/4amp of NaHCO3 in 1 lt of D5% and infuse at rate of 10-15 ml/kg/hr. (25ml of 7.5% NaHCO3 contains 22mEq NaHCO3). Bicarbonate haemodialysis can be done in patients with serum concentration of salicylates > 80mg /dl, refractory acidosis, severe CNS symptoms, progressive clinical deterioration, pulmonary edema, renal failure.
  88. 106. 5. Renal failure At gfr <20ml/min, inability to excrete H+ with retention of anions – PO 4 3- , SO 4 2+ results in increased anion gap acidosis. The unmeasured anions replace HCO3 - which is consumed as a buffer. Hyperchloremic metabolic acidosis (normal anion gap) develops in milder cases (gfr = 20-50ml/min). Correction of severe acidosis with alkali therapy in renal failure patients carries risk of volume overload. In such patients, dialysis can be used.
  89. 107. II ] Normal anion gap acidosis The hallmark of this disease is low HCO 3 of metabolic acidosis with hyperchloremia so that anion gap remains normal 1. GI loss of bicarbonate Diarrhea or pancreatic damage can result in HCO 3 loss due to increased secretion and decreased absorption. Hyperchloremia occurs because the ileum and colon secrete HCO 3 - in one to one exchange for Cl - by counter transport. The resultant volume contraction causes further increased Cl - retention by kidney in setting of decreased HCO 3 . Correction of hypvolemia and hypokalemia are the most important measures. Correction of acidosis with NaHCO 3 is required only in selected patients with severe acidosis.
  90. 108. 2. Renal tubular acidosis a. Classic distal (type 1) RTA Characterized by hypokalemic, hyperchloremic metabolic acidosis and is due to selective deficiency of H + secretion in distal tubules. Despite acidosis, Urinary pH is always above 5.5 Nephrocalcinosis, nephrolithiasis and bone disease are important clinical complications. Supplementation of bicarbonate (1-3mEq/kg/day) is essential. Potassium salt is given to correct hypokalemia.
  91. 109. b. Proximal (type 2) RTA characterized by hypokalemic, hyperchloremic metabolic acidosis due to a selective defect in proximal tubular ability to reabsorb filtered HCO 3 . During early stage, when HCO 3 is >18 mEq/lt, urine is alkaline but can be acidic when plasma HCO 3 <15-18 mEq/lt. Treatment is to treat the underlying disorder. If alkali therapy is needed, dose is quite large (10-15mEq/lt). Supplement potassium adequately to avoid hypokalemia. Thiazide diuretics can also be helpful.
  92. 110. c. Type IV RTA It is characterised by a disturbance in distal nephron function that impairs renal excretion of both H + and K + , so there is hyperchloraemic normal anion gap acidosis with hyperkalemia. Magnitude of hyperkalemia and acidosis are disproportionately severe for the observed degree of renal insufficiency. In Type IV RTA, mild to moderate chronic renal failure is almost always present. Urine pH can be <5.5. Urinary ammonium excretion is depressed.
  93. 111. Urinary anion gap to assess hyperchloremic metabolic acidosis – Metabolic acidosis   NH 4 Cl excretion by the kidney Urinary anion gap reflects the ability of the kidney to excrete NH 4 Cl. Urinary anion gap = Na + + K + - Cl - 80 - NH 4 + Normally urinary anion gap is zero or positive with a value of 30-50 (mmol/lt). It is useful to differentiate between gi and renal cause of hyperchloremic acidosis. If the cause is gi HCO 3 loss, urinary anion gap is negative because of increased NH 4 Cl excretion by kidney. In RTA, with impaired NH 4 Cl excretion, urinary AG is positive.
  94. 112. In contrast to urinary NH 4 + excretion, measurement of urine pH cannot reliably distinguish acidosis of renal or extrarenal origin. An acidic urine pH does not necessarily indicate increase in net acid excretion. With a significant reduction in the availability of ammonium to serve as a buffer, only a small amount of distal H + secretion will lead to a maximal reduction in urine pH. In this setting, pH of the urine is acidic but the quantity of H + excretion is insufficient of meet daily acid production. By contrast, alkaline urine doest not necessarily imply a renal acidification defect. In conditions where availability of NH 4 + is not limiting, distal H + secretion can be massive and yet the urine remains relatively alkaline due to buffering effects of NH 4 + .
  95. 113. <ul><li>METABOLIC ALKALOSIS </li></ul><ul><li>pH > 7.45 </li></ul><ul><li>High HCO 3 </li></ul><ul><li>The most useful factors to determine etiology of metabolic alkalosis are – </li></ul><ul><li>ECF volume </li></ul><ul><li>Blood pressure </li></ul><ul><li>Urinary chloride concentration </li></ul><ul><li>Serum potassium </li></ul><ul><li>Urinary chloride differentiates metabolic alkalosis into two major groups. </li></ul>
  96. 114. Causes of Metabolic Alkalosis Saline responsive (Urine chloride <15 mEq/L) Saline resistant (Urine chloride > 20mEq/L) ECF volume depletion Vomiting / Gastric suction Diuretics Hypercapnia correction No ECF vol. Depletion NaHCO 3 infusion Multiple transfusion Normal or increased ECF Vol Hypertensive Hyperaldosteronism Cushing’s syndrome Normotensive Bartter’s syndrome Severe K + depletion
  97. 115. <ul><li>Clinical features </li></ul><ul><li>CNS - Neuromuscular excitability, paresthesia, light headache, carpopedal spasm. </li></ul><ul><li>CVS - Hypotension, cardiac arrhythmias </li></ul><ul><li>Others - Weakness, postural dizziness, muscle cramps. </li></ul><ul><li>Respiratory - Compensatory hypoventilation may cause hypoxia in patients with preexisting lung disease. </li></ul>
  98. 116. <ul><li>Treatment </li></ul><ul><li>A . Treat the underlying cause </li></ul><ul><li>B . Saline responsive alkalosis </li></ul><ul><li>adequate correction of volume, chloride and K + deficit. </li></ul><ul><li>IV isotonic saline with KCl or isolyte G are given. </li></ul><ul><li>H 2 inhibitors or PPI reduce gastric acid secretion and minimize further H + loss. </li></ul><ul><li>If alkalosis is due to diuretics, dose reduction may be needed. KCl supplementation, spironolactone or carbonic anhydrase inhibitors can be used. </li></ul><ul><li>In rare cases, diluted HCl can be given IV (0.1N HCl). It can cause thrombophlebitis. So should be infused in large veins. </li></ul>
  99. 117. 6. Dialysis can be useful in occasional patients with severe metabolic alkalosis, volume overload and renal failure. C. Saline resistant – Specific treatment of underling cause like surgical treatment for pituitary tumour or adrenal adenoma, or supportive treatment, like spironolactone, correction of hypokalemia, sodium restriction.
  100. 118. <ul><li>Respiratory acidosis </li></ul><ul><li> PaCO 2 </li></ul><ul><li> pH < 7.35 </li></ul><ul><li>In most cases, hypoxemia occurs earlier and is more prominent than hypercapnia. </li></ul><ul><li>All patients with hypercapnia, who are breathing room air are hypoxic. </li></ul><ul><li>In chronic hypercapnia, hypoxemia is the primary stimulus to respiration. So, rapid and excessive correction of hypoxemia with uncontrolled oxygen can cause extreme hypercapnia, which can lead to neurological symptoms. . </li></ul>
  101. 119. Causes of Respiratory Acidosis CNS depression Drugs (anesthesia, sedative) Infection, Stroke Neuromuscular impairment Myopathy, myasthenia gravis, polymyositis, hypokalemia Ventilation restriction Rib fracture, pneumothorax, haemothorax Airway Obstruction, asthma Alveolar diseases COPD, pulmonary oedema, ARDS, pneumonitis Miscellaneous Obesity, hypoventilation
  102. 120. <ul><li>Clinical features </li></ul><ul><li>Features of underlying primary disorder’ </li></ul><ul><li>CNS – anxiety, headache, dysopnea, psychosis, hallucination and coma can be caused by acute severe hypercapnia. Chronic hypercapnia can lead to sleep disturbances, personality changes, tremors, myoclonic jerkes. Increased CSF pressure may cause papilloedema. </li></ul><ul><li>CNS manifestations are more with respiratory acidosis and less with metabolic acidosis. </li></ul>
  103. 121. <ul><li>Treatment </li></ul><ul><li>A. General measures </li></ul><ul><li>Treat the underlying cause promptly </li></ul><ul><li>Adequate oxygenation </li></ul><ul><li>If a patient of chronic hypercapnia develops sudden increase in PaCO 2 , search for the aggrevating factor. Vigorous treatment of pulmonary infection, bronchodilator therapy and removal of secretions. </li></ul>
  104. 122. B. Oxygen therapy Oxygen therapy is like a “Double edged Sword”. In acute respiratory acidosis, major threat to life is hypoxia and not hypercapnia. So O 2 supplementation is needed. In chronic hypercapnia, O 2 therapy should be instituted cautiously and in lowest possible concentration since hypoxia may be primary and only stimulus to respiration. C. Mechanical ventilation In acute respiratory acidosis, early use of mechanical ventilator is more appropriate. While in chronic respiratory acidosis, more conservative approach is admirable, because of greater difficulty in weaning such patients from ventilators.
  105. 123. <ul><li>Indications </li></ul><ul><li>Unstable, symptomatic or progressively hypercapnic (PaCO 2 > 80mmHg) patients. </li></ul><ul><li>Signs of muscle fatigue apparent, start MV before respiratory failure occurs. </li></ul><ul><li>Refractory severe hypoxia or apnea. </li></ul><ul><li>Depression of respiratory center (e.g. drug overdose) </li></ul><ul><li>In patients with chronically  PaCO 2 , rapid correction of hypercapnia with MV may lead to post hypercapnic alkalosis, which can be detrimental. So, correction of hypercapnia should be done gradually. </li></ul>
  106. 124. D. Alkali therapy Avoid alkali therapy except in patients with associated metabolic acidosis, severe acidaemia (pH<7.15), severe bronchospasm, as alkali therapy restores responsiveness of bronchial musculature to  agonists. Respiratory alkalosis  PaCO 2 ­  pH (>7.45) Etiology Respiratory alkalosis is the most frequently encountered acid base disorder
  107. 125. Causes of Respiratory Alkalosis <ul><li>Hypoxemia </li></ul><ul><li>Pulmonary disease : Pneumonia, interstitial fibrosis, emboli and oedema </li></ul><ul><li>CHF, hypotension or severe anaemia </li></ul><ul><li>High altitude residence </li></ul><ul><li>Pulmonary diseases </li></ul><ul><li>Direct stimulation of the medullary respiratory center </li></ul><ul><li>Psychogenic or voluntary hyperventilation, pain, pregnancy </li></ul><ul><li>Hepatic failure, gram negative septicemia </li></ul><ul><li>Salicylate intoxication </li></ul><ul><li>Rapid correction of metabolic acidosis </li></ul><ul><li>Neurological disorders, accidents, pontine tumour </li></ul>
  108. 126. Clinical features Clinical features vary with severity, rate of onset and underlying disorder. The mortality increase is in direct proportion to the severity of hypocapnia. PaCO 2­ below 20-25 mmHg carries a grave prognostic sign, specially in critically ill patients. Common features are :- Light headache, tingling of the extremities, circumoral anaesthesia, cardiac arrhythmias, tetany or seizures.
  109. 127. <ul><li>Treatment </li></ul><ul><li>Treatment of underlying cause </li></ul><ul><li>Mild alkalosis with few symptoms needs no treatment. </li></ul><ul><li>As hypoxemia is the common cause of hyperventilation, O 2 supplementation is essential along with etiological diagnosis and treatment. </li></ul><ul><li>In absence of hypoxemia, hyperventilation needs reassurance and rebreathing in a paper bag. </li></ul><ul><li>Pretreatment with acetazolamide minimizes symptoms due to hyperventilation at high altitude. </li></ul>
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