Arterial Blood GAS Analysis.pptx

Arterial Blood GAS Analysis.pptx

1. Arterial Blood GAS Analysis (ABG) In Pediatric Practice

2. Arterial Blood GAS Analysis (ABG) Must for every pediatrician, interested in treating critically ill pts. Acute disorders of RS, CVS, GI, Renal  Acid - base disturbances are inevitable ↓ Serious acid – base disturbances can co exist without significant clinical manifestations ↓ Early identification  Prompt efforts to maintain normal homeostasis till the organ function recovers.

3. ABG Reveals, Oxygenation status Adequacy of ventilation Acid – base balance Plays significant role in, Documenting and monitoring respiratory failure, especially during oxygen and ventilator therapy

4. Normal Metabolism & its Dysfunction Cellular function - dependent on glucose, O 2 and water Tissue oxidation  Volatile acids (Carbonic acid) + Products of Intermediary metabolism  Fixed acids [ Sulphuric acid, Phosphoric acid, Lactic acid, Keto acid] ↓ General Circulation ↓ Volatile acids are eliminated by RS Fixed acids by Renal System Buffers

5. H + Homoestasis Normal H +  40 nEq /L (Range  36 - 44 nEq /L) ↓ Deviation from range  impairment of vital organ functions Excessive accumulation of H + (Shock, Asphyxia, Ketoacidosis ) ↓ to be eliminated immediately ↓ Buffers and RS  within hours Renal (major role)  Delayed (within days) ↓ water transports H + in non - toxic form H + Carbonic anhydrase Co 2 (Removed by lungs) Co 2 ( ventilatory failure) Kidneys as H +

6. H + Concentration & Co 2 Organic compounds Co 2 ↓ Removed by alveolar ventilation Normal PaCo 2  40 mm of Hg (Range  36 – 44 mm of Hg) PaCo 2 > 44 mm of Hg  Respiratory acidemia ( Ventilatory failure) PaCo 2 < 36 mm of Hg  Respiratory alkalosis Paco 2  . Sensitive index of alveolar ventilation . Inversely related to alveolar ventilation . Controlled by chemoreceptors in hypothalamus oxidized During intermediary metabolism

7. 95% of Co 2 produced is transported by the RBC and 5% by plasma ↓ 99.9% as physically dissolved (dco 2 ) 0.1% as chemically dissolved (H 2 Co 3 ) ↓ The pressure exerted by dco 2  PaCo 2 ↓ Total Co 2 (Tco 2 )  dCo 2 + H 2 Co 3. In RS disturbances, PaCo 2 is not affected initially as diffusion capacity of Co 2 20 times > O 2 For every 20 mm of Hg ↑ PaCo 2  ↓ pH 0.1 For every 10 mm of Hg ↓ PaCo 2  ↑ pH 0.1

8. H + Concentration and HCo 3 - At normal H + conc. Of 40 nEq ./L (pH 7.4), HCo 3 - level is 24 mEq ./L, range  22 - 26 meq ./L. HCo 3 - < 22 meq ./L  Metabolic acidosis [Acute diarrhoea , RTA, Addition of lactic acid and Ketoacids ] HCo 3 - > 26 meq ./L  Metabolic Alkalosis [Persistent vomiting, ↑ RAT loop diuretics] HCo 3 - homeostasis is regulated by kidneys by reabsorption /regeneration of HCo 3 -

9. H + Concentration and pH pH  - ve logarithm of H + conc. ↓ No units denotes acidity/alkalinity Amount of H + in our body is too small to express easily, (0. 000 000000 40) 40 nEq /L ↓ pH notation by Henderson Normal pH  7.4 H + conc. 40 nEq ./L range  7.36 to 7.44 Lower pH  Higher H + conc.  Acidosis Higher pH  lower H + conc.  Alkalosis

10. Relationship of pH with Co 2 & HCo 3 - Henderson - Hasselbalch Equation pH = = ↓ It is the ratio of PCo 2 to HCo 3 that really decides the pH more than the absolute value. HCo 3 - PaCo 2 Renal compensation Pulmonary Compensation

11. Acid - Base Disorder Ultimate aim of the body is to maintain the pH within near normal limits. Main two types of mechanisms Chemical Buffers Extracellular First line defense Act within min. Bicarbonate S. Proteins Intracellular Act as a slower rate Within hours Intracellular proteins Hb Phosphates Physiological Compensation Lungs Kidneys Chemical buffering is not enough ↓ Physiological Compensation starts

12. Acid - Base Disorder When HCo 3 - loss occurs from body (Primary event) ↓ RS comes to rescue  eliminating Co 2 (compensatory) ↓ till pH  N a long with buffers (12 – 24 hours) When Co 2 is accumulated in the body (Primary event) ↓ Kidneys retain HCo 3 - (compensatory) & along with buffers normalize the pH (3 to 5 days) Acid Base Disorder may be, - Acute (uncompensated) - Subacute (Partially Compensated) - Chronic (Fully compensated)

13. Acid - Base Disorder Stages of Compensation Primary Disturbance pH HCo 3 - PCo 2 Metabolic acidosis Acute ↓ ↓ N Partially Compensated ↓ ↓ ↓ Fully Compensated N ↓ ↓ Respiratory Acidosis Acute ↓ N ↑ Partially Compensated ↓ ↑ ↑ Fully Compensated N ↑ ↑

14. Acid - Base Disorder Stages of Compensation Primary Disturbance pH HCo 3 - PCo 2 Respiratory Alkalosis Acute ↑ N ↓ Partially Compensated ↑ ↓ ↓ Fully Compensated N ↓ ↓ Metabolic Alkalosis Acute ↑ ↑ N Partially Compensated ↑ ↑ ↑ Fully Compensated N ↑ ↑

15. Metabolic Acidosis Commonest acid base disorder Mechanisms: - Loss of HCo 3 - (GIT/Kidney) - Addition of acids (LA/KA) - Administration of fluid devoid of HCo 3 - (TPN/massive transfusion) Metabolic acidosis - With ↑ anion gap - With normal anion gap.

16. Anion Gap According to electrochemical law, equal number of anions balance equal number of cations giving electrical neutrality. A small amount of anion that can not be measured by biochemical investigations is named as anion gap. (Na + + K + ) = ( Cl - + HCo 3 - ) + (Unmeasured anions) (Anion gap) (135 + 04) = (100 + 24) + 8 to 16

17. Metabolic Acidosis In some types  addition of acids ↓ ↓ HCo 3 - ↓ ↑ Unmeasured anions without any alteration of Cl - ↓ . Metabolic Acidosis with increased anion gap . Normochloremic acidosis Loss of HCo 3 -  ↑ Cl - ↓ Metabolic acidosis with normal anion gap Hyperchloremic acidosis ↓ HCo 3 - correction judiciously Administration of HCo 3 - may be hazardous

18. Correction of acidosis should be attempted only when: . HCo 3 - < 15 meq ./L . pH 7.2 . Base deficit 10 mmol /L Overzealous correction of acidosis with HCo 3 - ↓ (Hypertonic solution ) Shifting of oxygen - Hb dissociation curve to the left  poor O 2 release at tissue Hypokalemia Hypocalcemic tetany IVH Hypernatremia HCo 3 - correction 0.6 * Body wt (kg) * (15 – measured HCo 3 - ) ↓ . ½ dose immediately by slow IV after dilution with 5% D . Rest to be added in maintenance fluid over 24 hours

19. Metabolic Acidosis Ketoacids . Diabetes Mellitus . Starvation Sulphuric / Phosphoric acids . Renal failure Increased anion gap ( Noramochloremic acidosis) Lactic acidosis Shock Asphyxia Cyanide poisoning Salicylate poisoning Organic acidemia Inborn errors of carbohydrate & pyruvate metabolism Normal anion gap ( Hyperchloremic acidosis) Diarrhoea RTA Parenteral alimentation Rapid ECF expansion CaCl 2, Mgcl 2, NH 4 Cl Small bowel or biliary fistula

20. Metabolic Alkalosis Acid loss GIT loss Vomiting N – G tube aspiration Mineralo corticoid activity Cushing’s syndrome Hyperaldosteronism Bartter’s syndrome Liquoric carbenoxolone Alkali gain Rapid HCo 3 - correction Massive transfusion (citrate) Excessive antacids ECF loss Cl - > HCo 3 - Cystic fibrosis Massive Diuresis

21. Metabolic Alkalosis Clinical presentation: Shallow respiration (attempt to conserve Co 2 ) Altered sensorium Muscle cramps Dys arrhythmias Tetany (due to low ionized calcium) Volume loss and or hypokalemia GFR is maintained Adequate ECF volume Normally functionind kidneys Excessive HCo 3 - eliminated ↓ production of NH 3 ↓ Normalizing basic pathology

22. Metabolic Alkalosis If ECF volume is not adequately maintained ↓ Low GFR ↓ HCo 3 - retention (alkali gain) + ↑ aldosterone production ↓ Loss of H + (acid loss) in exchange of Na + at distal convoluted tubule Hypokalemia  aggravates basic pathology ↓ Maintain adequate ECF volume + Serum K +

23. Metabolic alkalosis Resulting from ↑ aldosterone activity (saline resistant) ↓ Spirono lactone ACE inhibitors Amiloride Indomethacin Saline responsive M.Alk .  urine Cl - < 10 meq /L Saline resistant M. Alk .  urine Cl - > 10 meq ./L

24. Respiratory Alkalosis CVS . Cardiac failure CNS infections Trauma Sepsis Hypothyroidism Salicylate poisoning Pathological Lung Disease Obstructive Restrictive Embolus Physiologica Anxiety Fever Screaming Hysterical Mechanical ventilation Iatrogenic

25. Respiratory Alkalosis Mild respiratory disorders  Hypoxemia ↓ Oxygenation Failure [Type I Respiratory Failure] Hypoxic drive  Hyper ventilation ↓ Washing out CO 2 ↓ Respiratory alkalosis Correction of basic pathological condition + Prompt O 2 supplementation Hysterical breathing  Rebreathing in paper bag

26. Respiratory Acidosis Ventilatory Type II Failure Respiratory Obstructive Aspiration Croup FB Epiglottitis Asthma Bronchiolotis Paranchymal Pneumonia RDS Interstitial lung disease Pulmonary oedema Pleural Pleural effusion Pneumothorax Thoracic Cage . Flail chest . Scoliosis Neuromuscular Brain stem lesions Opium Poliomyelitis G B syndrome Myasthenia Gravis Botulism Picwickian syndrome

27. Oxygen Homeostasis Pao 2 normal  80 - 100 mm of Hg Newborn  40 – 70 mm of Hg Hypoxemia: Mild  Pao 2 60 - 80 mm of HG Moderate  Pao 2 40 - 60 mm of HG Severe  Pao 2 < 40 mm of HG Pao 2  O 2 level in arterial blood Adequacy of tissue oxygenation decides cellular metabolism Delivery of O 2 to tissues depends on, - Pao 2 - Circulation - Hb - Mitochondrial function Shift of O 2 - Hb dissociation curve to right

28. Practical Workup of ABG ABG Symbols and values: Term Symbol Normal Value Range Unit H + H + 40 36 – 44 nmol /L pH pH 7.4 7.36 – 7.44 - Co 2 tension PaCo 2 40 36 – 44 mm of Hg Base Excess BE -2 to 2 mmol /L Total Co2 TCo 2 25 23 - 27 mmol /L Actual HCo 3 HCo 3 24 22 – 26 nmol /L Standard HCo 3 SBC 24 22 – 26 mmol /L O 2 Saturation SaO 2 98 95 – 100 % O 2 tension PaO 2 95 80 – 100 mm of Hg

29. ABG Specimen Collection Preferred site: Radial artery at the wrist (adequate collaterals) Alternates: Popliteal , Branchial , Femoral Cleansing the Inj. Site: Iodine/Alcohol Heparinized syringe with 22 gauge needle - at 45 . angle Artery puncture: just 2 cm above the wrist crease Presence of air bubbles may increase O 2 values & lower Co 2 values. Estimation - immediately 0.05 to 0.1 ml of heparin for 1 ml of blood Local pressure for 3 - 5 min.

30. ABG Interpretation Step by step Approach pH: Acidosis/Alkalosis Respiratory/Metabolic Stages of compensation Oxygen status Simple disorder/Mixed disorder Acute/Chronic Laboratory Error

31. Step I: pH - Acidosis/Alkalosis Normal pH range: 7.36 to 7.44 pH < 7.36: Acidemia Ph > 7.44: Alkalemia Step II: Respiratory/Metabolic Acidemia due to ↑ PaCo 2 / ↓ HCo 3 - Alkalemia due to ↓ PaCo 2 / ↑ HCo 3 - In Respiratory Acidosis, Kidney regenerates HCo 3 - & ↑ HCo 3 - as a compensatory response in addition to hypervantilation

32. Metabolic acidosis is compensated by hyperventilation ( Kussmaul’s breathing) elimination of Co 2 increases the pH to alkaline side. Metabolic alkalosis occurs when HCo 3 - level exceeds the normal limits, which is compensated by hyperventilation to ↑ Co 2 level.

33. Step III: Stages of compensation Acute (Uncompensated stage): pH and PaCo 2 / HCo 3 - Abnormal Compensation occurs to normalize First body buffers (within minutes), Followed by Respiratory (within hours) And Renal System (within days). Sub acute (Partially Compensated): - pH  abnormal or near to Normal - Co 2 & HCo 3 - in same direction Chronic (Fully compensated): - pH  Normal - PCo 2 & HCo 3 - abnormally altered

34. Stage IV: Oxygenation status PaO 2 Normal value, In children and adults  80 – 100 mm of Hg In newborn  40 – 70 mm of Hg If the child is critically ill ĉ cardiopulmonary problem, 100% O 2 irrespective of oxygen status  O 2 supplementation below 60% to avoid O 2 toxicity (BPD & RF) If Hb is inadequate, final delivery of O 2 to the tissues will be compromised.

35. Stage V: Simple/Mixed Disorder Simple disorder: PaCo 2 & HCo 3 - change in same direction ↓ Change in trend  Mixed disorder The difference between TCo 2 & HCo 3 - is > 1.2 in addition to metabolic cause ↓ Underlying respiratory disturbance Both actual HCo 3 - & standard HCo 3 - are not the same  In addition to respiratory Cardiopul . arrest Acute severe Asthma Shock RDS Diuretic Salicylate poisoning Decomp . Liver Disorders Metabolic component → Mixed disturbances

36. Stage VI: Acute/Chronic Disorder Compensation Metabolic acidosis: For every 1 meq ./L ↓ in HCo 3 - , PaCo 2 ↓ by 1 mm of Hg (1 – 1.5) Metabolic alkalosis: For every 1 meq ./L ↑ in HCo 3 - , PaCo 2 ↑ by 1 mm of Hg (0.5 – 1) Respiratory acidosis: Acute: For every 1 mm ↑ PaCo 2, HCo 3 - ↑ by 0.2 meq ./L Chronic: For every 1 mm ↑ PaCo 2, HCo 3 - ↑ by 0.4 meq ./L Respiratory alkalosis: Acute: For every 1 mm ↓ PaCo 2, HCo 3 - ↓ by 0.2 meq ./L Chronic: For every 1 mm ↓ PaCo 2, HCo 3 - ↓ by 0.5 meq ./L

37. Stage VII: Laboratory Error Henderson Hassel bach equation, H ( nmol /L) = 24 (PCo 2 / HCo 3 - ) ↓ If two are known, third can be calculated ↓ If there is discrepancy between measured value & calculated values ↓ Laboratory Error ?