Acid base abnormalities and blood gas analysis for UG

Blood gas analysis, paediatrics, sample scenarios,icu care

1. INTERPRETATION- ABG/ VBG Dr Avinash Kumar Jha MBBS(Gold Medalist),DNB, PGPN(Boston) Assistant Professor Paediatrics

2. GOAL of this presentation??? Simple and bedside approach to ABG report

3. Physiology of Acid base balance Hydrogen ion concentration influences almost all enzyme systems in the body. The body’s respiratory and renal systems coordinate to regulate H+ homeostasis by regulating HCO3- and PCO2. Once derangement occurs, H+ concentration is corrected in a timely and stepwise approach starting with chemical buffers, followed by pulmonary ventilation and finally renal control acid base excretion Ganong’s review of medical physiology, 24e

4. Defense against changes Three primary systems: Chemical acid base buffer system acts within fraction of a second. Respiratory system acts within few minutes. Renal system Slow to respond, but the most powerful of the acid base regulatory systems. Ganong’s review of medical physiology, 24e

5. Chemical Buffers Bicarbonate buffer – major buffer Phosphate - Major role in buffering renal tubular fluid and intracellular fluids Proteins – major intracellular buffer. Hemoglobin is one of the important protein buffer in our body Ganong’s review of medical physiology, 24e

6. Pulmonary regulation Lungs respond by altering the depth and rate of ventilation Peripheral chemoreceptors respond within minutes in change to pH, pCO2 and pO2 Central receptors respond to pCO2 slowly but strongly Begins in the first hour and fully established by 24 hours West JB (2005) Respiratory physiology: the essentials, 7 th ed. Philadelphia: Lippincott Williams & Wilkins, ix, 186 Pierce NF, Fedson DS, Brigham KL, et al. (1970) The ventilatory response to acute base deficit in humans. Time course during development and correction of metabolic acidosis. Ann Intern Med 72(5): 633–40

7. Renal regulation Renal compensation begins in the first day and fully established in 3 to 5 days Three fundamental mechanisms: reabsorption of filtered bicarbonate ions secretion of hydrogen ions production of new bicarbonate ions. Controls acid base balance by excreting either an acidic or basic urine. Ganong’s review of medical physiology, 24e

8. H+ ATPase Na- K ATPase Na- H antiporter Na-HCO3 co trasnsporter Nelson, Textbook of pediatrics, 20e

9. Arterial sampling Required for ABG Obtained by percutaneous needle puncture or indwelling arterial catheter Common Sites: Radial artery (mc site) Femoral artery Brachial artery Dorsalis pedis artery Complications of Needle Puncture Persistent bleeding, bruising, injury to blood vessel and Thrombosis leading to distal circulation block The Harriet Lane handbook, 20e Fleisher G, Ludwig S. Textbook of Pediatric Emergency Medicine. 6th ed. Baltimore: Williams & Wilkins, 2010.

10. Alternative to ABG  VBG !!! A VBG can be performed using peripheral venous sample (obtained by venipuncture) central venous sample (obtained from a central venous catheter), or mixed venous sample (obtained from the distal port of a pulmonary artery catheter )

11. Clinical implications of VBG A VBG measures the venous oxygen tension (PvO2), carbon dioxide tension (PvCO2), acidity(pH), oxyhemoglobin saturation (SvO2 ) and serum bicarbonate (HCO3) concentration PvCO2 , venous pH, and venous serum HCO3 concentration are used to assess ventilation and/or acid- base status SvO2 is used to guide resuscitation during severe sepsis or septic shock , a process called early goal directed therapy Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2016

12. PvO2 has no practical value. It is not useful in assessing oxygenation because oxygen has already been extracted by the tissues by the time the blood reaches the venous circulation. The inability of a VBG to measure oxygenation is the major drawback compared with an ABG.To overcome this limitation,VBGs are often considered in combination with pulse oximetry. Byrne AL, Bennett M, Chatterji R, et al. Peripheral venous and arterial blood gas analysis in adults: are they comparable? A systematic review and meta- analysis. Respirology 2014; 19:168

13. ABG & VBG values Rao MS, Nagendranath V. Arterial blood gas monitoring. Indian J Anaesth 2002;46:289- 97

14. Central venous blood gases are preferred because their correlation with arterial blood gases is the most well- established by research and clinical experience. Peripheral venous blood gases are an alternative for patients who do not have central venous access. Kelly AM, Klim S, Rees SE. Agreement between mathematically arterialised venous versus arterial blood gas values in patients undergoing non- invasive ventilation: a cohort study. Emerg Med J 2014

15. Central Vs Peripheral Byrne AL, Bennett M, Chatterji R, et al. Peripheral venous and arterial blood gas analysis in adults: are they comparable? A systematic review and meta- analysis. Respirology 2014; 19:168. Kelly AM, Klim S, Rees SE. Agreement between mathematically arterialised venous versus arterial blood gas values in patients undergoing non- invasive ventilation: a cohort study. Emerg Med J 2014; 31:e46 .

16. Care of the specimen Pre- heparinised syringe to be used. FLUSH with atleast 0.5ml heparin and discard ENSURE no air bubbles. Williams AJ. ABC of oxygen: assessing and interpreting arterial blood gases and acid- base balance. BMJ 1998; 317:1213

17. IFCC recommendations Heparin should be taken to lubricate the inner wall of syringe Heparin should be expelled completely Atleast, 20 times the dead space volume of blood should be collected Use of concentrated heparin, reduces ph Dilutional effect can cause fall in pco2 and bicarbonate Syringes with minimal liquid heparin are most appropriate for studying BG parameters as they have the least effect on these parameters.

18. Patients body temperature affects the affects the value of PCO 2 and HCO 3- . pH increases and both PaO 2 and PaCO 2 decrease as temperature declines. Shapiro et al. (1994) Clinical application of blood gases, 5th ed. St. Louis: Mosby- Year Book, p. 128

19. Should be Transported at the EARLIEST and preferably maintaining cold chain. Shapiro et al. (1994) Clinical application of blood gases, 5th ed. St. Louis: Mosby- Year Book, p. 128

20. Henderson-Hasselbach equation Ganong’s review of medical physiology, 24e

21. T e r m i n o l o g y Acidemia — An arterial pH below the normal range (less than 7.35). Alkalemia — An arterial pH above the normal range (greater than 7.45). A c i do s i s — A p r o c ess t h a t t e nd s t o l o w e r t he e x t r a c e llula r fluid p H ( h y d r o g en i o n concentration increases).This can be caused b y a fall i n t he se r u m bicarbonate ( H C O 3 ) concentration and / o r a n e l e v a ti o n i n P C O 2 . Alkalosis — A process that tends to raise the extracellular fluid pH (hydrogen ion concentration decreases).This can be caused by an elevation in the serum HCO3 concentration and/or a fall in PCO2. Nelson textbook of pediatrics, 20 e

22. Simple Acid Base disorders Metabolic acidosis – A disorder that reduces the serum HCO3 concentration and pH Metabolic alkalosis – A disorder that elevates the serum HCO3 concentration and pH Respiratory acidosis – A disorder that elevates the arterial PCO2 and reduces the pH. Respiratory alkalosis – A disorder that reduces the arterial PCO2 and elevates the pH. Mixed acid- base disorder – The simultaneous presence of more than one acid-base disorder. Nelson textbook of pediatrics, 20 e

23. What machine measures? pH – Measured indirectly with an electrode tip which determines the volltage using a reference potential, calibrated in pH units; where voltage is proportional to concentration of hydrogen ions PaCO2 - measured using a chemical reaction that consumes CO2 and produces a Hydrogen ion, which is sensed as change in pH PaO2 - measured using oxidation-reduction reactions that generate measurbale electric currents

24. Understanding the parameters Base Excess (BE) BE refers to actual base excess in variance from total buffer base(BB). Amount of strong base (negative base excess, or “base deficit”) or strong acid (positive base excess) in mmol/L that would be needed to restore a pH of 7.4 to a liter of whole blood equilibrated at PCO2 = 40 mm Hg. It excludes the effect of acute changes in PCO2, so it loses accuracy if PCO2 is abnormal. It should not be used in critically ill patients

25. Normal BB is 48-49 mmol/liter BB constituted by bicarbonate (50%), hemoglobin (25%) and others (proteins, phosphate, sulphate – 25%) If BE is negative (eg -8) it reflects base deficit: metabolic acidosis If BE is positive (eg +8) it reflects base excess: metabolic alkalosis

26. Standard Base Excess Similar to BE but involves in-vivo measurements which involves equilibration with entire ECF compartment and not just Blood In vivo buffering capacity is lower as interstitial compartment is free of Hemoglobin Since interstitial compartment is 3 times that of blood, correction for hemoglobin is essential. SBE is thus the BE adjusted for the hemoglobin buffer Correction of metabolic disorders should therefore be based on SBE and not on BE

27. Derived parameters BO2e = Oxygen capacity of hemoglobin. The maximum concentration of O2 bound to Hb in blood, saturated so that all deoxyHb is converted to oxyHb ctO2e = Total oxgen concentration of blood (O2 content) Anion Gap: (K+) Concentration difference of K+ + Na+ and Cl– + HCO3- Anion Gap: Concentration difference of Na+ and Cl– +HCO3- Hct: Fraction of the volume of erythrocytes in the volume of whole blood P50e = Oxygen tension at 50% saturation of blood ctCO2(B) = concentration of total CO2 of whole blood (CO2 content) Radiometer ABL 800 manual

28. Harrison’s internal medicine, 18e

29. steps for Successful blood gas analysis Harrison 19 th edition

30. Step 1 Look at the pH Is the patient Or Normal (7.35-7.45) acidemic pH<7.35 alkalemic pH>7.45 Harrison 19 th edition

31. Step 2 Look at the pCO2 (Normal =35- 45mmHg) pH and PCO2 change in opposite direction in respiratory problem. pH and PCO2 change in same direction in metabolic problem.

32. Step 2 Disorder pH pCO2 Metabolic Respiratory DR - Different MS - Metabolic Respiratory Same

33. Step 3 Compensation (CO2 and HCO3) Body tries to compensate to normalise pH HCO3 and CO2 always move in the same direction . Pulmonary regulation – begins in first hour, fully established by 24 hours. However only 50-75% effective in restoring the pH. Renal acid regulation- starts late. By the end of 1 st day, fully established by 3- 5 days

34. Check how much compensation?? Metabolic acidosis Expected PaCO2 = (1.5 × HCO3) +8 + 2 If actual PaCO2 is more than expected PaCO2 = additional respiratory acidosis If actual PaCO2 is equal to expected PaCO2 = compensated metabolic acidosis If actual PaCO2 is less than expected PaCO2 = additional respiratory alkalosis Harrison 19 th edition

35. Check how much compensation?? Metabolic alkalosis Expected PaCO2 = 0.7( HCO3) +20 + 2 If actual PaCO2 is more than expected PaCO2 = additional respiratory acidosis If actual PaCO2 is equal to expected PaCO2 = compensated metabolic alkalosis If actual PaCO2 is less than expected PaCO2 = additional respiratory alkalosis Harrison 19 th edition

36. Harrison 19 th edition

37. Disorder Primary Change pH Pco2 Hco3 Compensation Metabolic Acidosis Co2 Metabolic alkalosis Co2 Respiratory Acidosis Hco3 Respiratory Alkalosis Hco3

38. Step 4 Acute Vs chronic PaCO2 change of 10 mmHg causes a pH change of Acute change Chronic change 0.08 0.03 Harrison 19 th edition

39. Step 5 Measured cations – Measured anions

40. HIGH ANION GAP METABOLIC ACIDOSIS NORMAL ANION GAP METABOLIC ACIDOSIS Harrison 19 th edition

41. Normal anion gap acidosis Calculate urinary anion gap [Na] +[K] – [Cl] Normal anion gap UAG – neGUTtive UAG - positive Negative UAG – gastroenteritis , exogenous acid. Positive UAG -renal tubular acidosis .

42. High anion gap acidosis Measure osmolal gap and delta –delta Osmolal Gap = measured –calculated osmolality Addition of alcohols, proteins, lipids and mannitol increase the measured osmolality and thus increase serum osmolar gap. Increased serum osmolar gap with high anion gap metabolic acidosis is an indirect indication of Ethanol intoxication Methanol Ethylene glycol Harrison 19 th edition

43. Delta gap = (change in anion gap) - (change in bicarbonate) Interpretation of the generated ratio: - 6 = normal anion gap metabolic acidosis - 6 to 6 = mixed high and normal anion gap acidosis exists. over 6 = mixed high anion gap acidosis and metabolic alkalosis Interpretation of the generated ratio: <1 = mixed high and normal anion gap acidosis exists. 1.0 = purely due to a high anion gap metabolic acidosis >1.0= high anion gap acidosis with pre-existing metabolic alkalosis Harrison 18 th edition

44. Revise the steps … 1. Acidosis or alkalosis 2. Metabolic or respiratory 3. Compensation 4. Acute or chronic 5.Anion gap 6. AG and Bicarbonate for mixed. Golden rule of ABG Interpretation Always look at the patients condition

45. Case 1 A 6 months old female child weighing 3.5kg presented with multiple episodes of loose stools and vomiting for 2 days. There was a history of refusal to feed and reduced activity for 1 day. Mother complains that child has not passed urine for last 12 hours. On examination - Child is lethargic with sunken eyes and AF , dry oral mucosa ,delayed skin pinch .HR-160/min, RR- 42/min, feeble peripheral pulses with CFT>3 secs. BP- 60/40 mmHg. Systemic examination was normal ABG- pH- 7.1, HCO3- 12, pCO2 -20, paO2- 70, Lactate - 6.4, Na -130meq/l, K-3.2 meq/l, Cl- 94meq/l, S.creat-2.1mg/dl, BU- 92mg/dl

46. Interpretation ABG- pH- 7.1, HCO3- 12, pCO2 -20, paO2- 70, Lactate -6.4, Na -130meq/l, K-3.2 meq/l, Cl- 94meq/l, Acidosis Metabolic Expected CO2= (1.5× HCO3)+ 8 + 2 4. = 26 + 2 5. Anion gap = 24 (high anion gap) High anion gap metabolic acidosis with respiratory alkalosis (compensated)

47. Primary lesion pH Compensation Bicarbonate PaCO 2 METABOLIC ACIDOSIS HYPER VENTILATION BICARB CHANGES pH in same direction Low Alkali Three clicks

48. 1. Increased H+ production Ketoacidosis Lactic Toxins – Ethanol, salicylate Acid ingestion Decreased renal excretion of H+ Renal failure RTA I Loss of HCO3- Diarhhea RTA II Nelson 20e

49. HIGH ANION GAP METABOLIC ACIDOSIS NORMAL ANION GAP METABOLIC ACIDOSIS Harrison 19 th edition

50. Case 2 9 year female child presented to RR with history of fever for last 4 days, pain abdomen 2 days, vomiting 5- 6 episodes and fast breathing since morning. She had past history of polyuria and polydipsia for last 1 month. O/E – conscious but lethargic. Rapid and deep breathing HR-120/min, RR-42/min, normal GCS.Spo2 on Rair- 94%. Dextrose – 520 mg/dl. Urine ketones - 4+. CBC/SE/KFT samples sent. ABG pH- 6.9,pCO2-24, HCO3 -5 mEq/l, lac - 4.2,Na- 132,K-3.2, cl- 96.

51. Interpretation ABG- pH- 6.9,pCO2-20 , HCO3 -6 mEq/l, lac -4.2,Na-132,K- 3.2, cl- 96 Acidosis Metabolic Expected CO2= (1.5× HCO3)+ 8 + 2 = 17 + 2 1. Anion gap = 2. Na - (Cl+HCO3) 30(high anion gap) High anion gap metabolic acidosis with respiratory alkalosis(compensated)

52. High anion gap metabolic acidosis

53. Case 3 A 7 month old child weighing 4kgs was brought to RR with complains of vomiting and fast breathing from 2 days . No history of fever , cough, coryza or cold. Antenatal history was uneventful. Baby was born a term with a birth weight of 2.8kgs. O/E child was lethargic, sunken eyes, and AF, oral mucosa ,skin pinch delayed. HR- 140/min, RR- 40/min ,feeble peripheral pulses with CFT>3 sec , BP – 60/48mmHg. Systemic examination was normal .u/o – 40 ml in last 4 hours. ABG- pH- 7.06,HCO3- 9,lac- 1.4,paO2-92, pCO2- 18 Na- 128,K- 2.8,cl-106,S.creat- 0.4,BU- 32 mg/dl Urine anion gap - positive

54. Interpretation ABG- pH- 7.06,HCO3- 9,lac- 1.4,paO2-92, pCO2- 18 Na-128,K-2.8,cl- 106 Acidosis Metabolic Expected CO2= (1.5× HCO3)+ 8 + 2 = 21.5 + 2 1. Anion gap = 2. Na - (Cl+HCO3) 13(normal anion gap) Normal anion gap metabolic acidosis

55. Case 4 2 months old male child weighing 3.3 kg presented to RR with multiple episodes of vomiting for last 8 days. No history of fever ,cough, cold. Child had a normal birth history with a birth weight of 3 kg. Antenatal scans revealed polyhydramnios. Child was symptomatic since day 15 of life. He had history of 4-5 episodes of vomiting/regurgitation of feeds. Child passes urine 14- 15 times a day O/E – child was lethargic, with signs of dehydration.AF normal . HR- 136/min, RR- 36/min,Spo2 – 94% on room air. ABG – pH- 7.58,pCO2- 70, pO2- 56, HCO3- 62.7,clac- 1.0. Na- 130, K – 1.3 , cl- 49 .Urine chloride levels - 77meq/l

56. Interpretation ABG – pH- 7.58,pCO2- 68, pO2- 56, HCO3- 63 ,clac- 1.0 Alkalosis Metabolic Expected CO2= (0.7× HCO3)+ 20 + 2 4. = 64 Urinary chloride levels Low- extrarenal causes High- renal causes Metabolic alkalosis with respiratory acidosis

57. Primary lesion pH Compensation Bicarbonate PaCO 2 METABOLIC ALKALOSIS HYPO VENTILATION BICARB CHANGES pH in same direction High Alkali Three clicks

58. Case 5 A 10 year old , diagnosed case of asthma presents to RR with difficulty in breathing. Child was started on MDI in the last visit, but had not been complaint to therapy. O/E – child was unable to speak in sentences. HR- 110/min, RR- 46/min, spO2 -86% on room air. R/S examination revealed B/L wheeze,B/L decreased air entry. ABG- Ph -7.11, PCO2- 74mmHg, paO2- 60 mmHg,HCO3- 27.5

59. Interpretation ABG – Ph -7.11, PCO2- 74mmHg, paO2- 60 mmHg,HCO3- 28 Respiratory Expected pH= (0.08 × change in 10 mmHg)for acute = 7.4- 0.272 =7.128 Chronic = 0.03 × change in 10 mmHg= =7.4 – .102=7.298 Expected HCO3= 1 meq/l for 10mmHg change. 2. = 24+3.4 Acute Respiratory acidosis

60. Respiratory Acidosis ALVEOLAR Hypoventilation CNS Depression Drugs Cerebral ischemia Sleep disorders Neuromuscular disorder Neuropathy Myopathy Chest wall abnormality Kyphoscoliosis Ankylosing spondylitis Pleural Abnormality Pneumothorax Pleural effusion Airway Obstruction FB/Tumor COPD/Severe asthma Parenchymal lung disease ILD Ventilator dysfunction

61. Primary lesion pH compensation PaCO 2 BICARB Respiratory acidosis CO CHANGES 2 pH in opposite direction High CO 2 Three clicks Wait for red circle

62. Case 6 2 year old male child presented with history of accidental ingestion of paint removal solution, known locally as NITRO around 9pm.Child had 2 episodes of vomiting within an hour following which child was drowsy and cyanosed. Drowsiness and cyanosis worsened. Clinical examination HR- 154/min, RR- 32/min, SpO2 – 80 on O2 by mask. Peripheral and central cyanosis present. ABG – Ph-7.411, Pco2-24.5, HCO3- 15.3,clac- 1.0, p02- 238mmHg

63. Primary lesion pH compensation PaCO 2 BICARB Respiratory alkalosis PaCO 2 CHANGES pH in opposite direction Low PaCO 2 Three clicks Wait for red circle

64. Respiratory Alkalosis Mainly due to hyperventilation CNS stimulation Meningitis Cerebrovascular accident Salicylate poisoning Hypoxemia Pneumonia Pulmonary edema Miscellaneous Sepsis Hepatic failure Mechanical hyperventilation Heat exposure

65. INDICATIONS OF ABG Respiratory distress - Moderate/ Severe Identification and monitoring of acid- base disturbances Renal Failure Cardiac disorders Neurological disorders

66. Take Home Pearls !!! ABG is absolutely indicated where Oxygenation needs to be assessed FiO2 (ventilated patients), Temperature have to be mentioned on ABG strip Step wise approach in diagnosing acid base disorder To become familiar with using anion gaps, osmolal gap and delta delta for better interpretation and narrowing of diagnosis Always correlate with patient’s clinical status

67. Acknowledgements

68. Case Muscular dystrophy . o mm Hg mm Hg mmol / L % mm Hg  Blood Gas Measured pH PaCO 2 PaO 2 Calculated HCO 3 act O 2 Sat PO 2 (A - a) PO 2 (a / A) Entered FiO 2 Report 37.0 C 7.301 76.2 45.5 Data 35.1 78 9.5 0.83 Data 21 % pH <7.35 :acidemia Res. Acidemia : High PaCO 2 and low pH Hypoxemia Normal A- a gradient D CO 2 =76- 40=36 Expected D pH for ( Acute ) = .08 for 10 Expected ( Acute ) pH = 7.40 - 0.29=7.11 Chronic resp. acidosis Hypoventilation Chronic respiratory acidosis With hypoxia due to hypoventilation Five clicks 6 year old male with progressive respiratory distress

69. Anion gap correction Adjusted AG in hypoalbuminemia = Observed AG + [2.5(normal albumin − observed albumin)].

70. Case 8- year- old male asth tired looking; on 4 L NC. o mm mm 3 days of cough, dyspnea Hg and orthopnea not Hg responding to usual bronchodilators. Report 37.0 C 7. 24 49.1 66.3 Data 18.0 mmol / L 92 m Hg  O/E: Respiratory distress; suprasternal and Blood Gas Measured pH PaCO 2 PaO 2 Calculated HCO 3 act O2 Sat PO 2 (A - a) PO 2 (a / A) Entered FiO 2 Data 30 % pH <7.35 ; acidemia 3 PaCO 2 >45; respiratory acidemia matic; p i O 2 = 715x.3=214.5 / p alv O 2 = 214- 49/.8=153 Wide A / a gradient Hypoxia % WITH INCREASE IN CO2 BICARB MUST RISE ? Metabolic acidosis + respiratory acidosis intercostal retraction; 30 × m 5 B i = ca r 1 b 5 o n a t e is low……… D CO 2 = 49 - 40 = 9 Expected D pH ( Acute ) = 9/10 x 0.08 = 0.072 Expected pH ( Acute ) = 7.40 - 0.072 = 7.328 Acute resp. acidosis 8- year- old male asthmatic with resp. distress Six clicks

71. o mm Hg Report 37.0 C 7.23 23 110.5 mm Hg Data 14 mmol / L % mm Hg  Blood Gas Measured pH PaCO2 PaO2 Calculated HCO 3 act O2 Sat PO2 (A - a) PO2 (a / A) Entered FiO2 Data 21.0 % pH <7.35 ; acidemia HCO3 <22; metabolic acidemia Last two digits of pH Correspond with co2 If Na = 130, Cl = 90 Anion Gap = 130 - (90 + 14) = 130 – 104 = 26 Case 8 year old diabetic with respi. distress fatigue and loss of appetite. Three clicks

72. Alveolar gas equation

73. Henderson-Hasselbach equation pH = pK + log ( HCO3/H2CO3) pK = 6.1 for H2CO3 Normal ratio of HCO3/H2CO3 = 20/1 Log 20 = 1.3 Normal pH =6.7 + 1.3 =7.4

74. Oxygen dissociation curve

75. o mm Hg mm Hg Report 37.0 C 7.46 28.1 55.3 Data 19.2 mmol / L g  Blood Gas Measured pH PaCO2 PaO2 Calculated HCO 3 act O2 Sat PO2 (A - a) PO2 (a / A) Entered Data FiO2 % mm H 24.0 % Case : 10 year old child with encephalitis pH almost within normal range Mild alkalosis PaCO 2 is low , respiratory low by around 10 ( Acute ) by .08 (Chronic ) by .03 BICARBINATURIA Bicarb looks low ? Is it expected ?

76. Sao2 is always measured and not calculated Co- oximeter; newer machines have cooximeter installed in them The traditional “blood gas machine“ measures only pH, PaCO 2, and PaO 2, , whereas the co-oximeter measures SaO 2 , carboxyhemoglobin, methemoglobin, and hemoglobin content. Newer “blood gas” consoles incorporate a co- oximeter, and so offer the latter group of measurements as well as pH, PaCO 2, and PaO 2 .

77. BACKGROUND PHYSIOLOGY – EFFECT OF ABNORMAL BODY TEMPERATURE ON BLOOD GAS PARAMETERS Henry’s fundamental law of gases determines that the solubility of oxygen and carbon dioxide in water varies with temperature; decreased temperature causes increased solubility of both oxygen and carbon dioxide. This general relationship between temperature and gas solubility is reflected in human physiology [6]. Hypothermia is associated with decreased p CO 2 and p O 2 , consequent on increased solubility, and hyperthermia is associated with increased p CO 2 and p O 2 , consequent on decreased solubility [7]. The temperature- dependent change in p CO 2 secondarily affects blood pH; hypothermia is associated with increased pH and hyperthermia with decreased pH [7]. Two other effects of change in body temperature are relevant to blood gas analysis: shifts in the oxyhemoglobin dissociation curve; and altered oxygen consumption and carbon dioxide production. Decreased body temperature (hypothermia) causes a leftward shift in the oxyhemoglobin dissociation curve, i.e. increases hemoglobin affinity for oxygen, whereas increased body temperature (hyperthermia) causes a rightward shift, i.e. decreases hemoglobin affinity for oxygen [8]. The change in hemoglobin affinity for oxygen induced by change in body temperature has the theoretical potential of impeding oxygen delivery to tissues in hypothermia and impeding binding of oxygen to hemoglobin at the lungs in hyperthermia. The sigmoidal shape of the oxyhemoglobin curve determines that the potential for these body temperature effects is greatest in those who are hypoxemic ( p O 2 < 10 kPa) [8]. Hypothermia is associated with reduced oxygen consumption and carbon dioxide production, whereas hyperthermia is associated with increased oxygen consumption and carbon dioxide production

78. Normal anion gap metabolic acidosis  Check urine anion gap neGUTive

79. Central cyanosis Peripheral cyanosis Methaemoglobinaemia