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![Normal Metabolism & its Dysfunction
• Cellular function - dependent on glucose, O2 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](https://image.slidesharecdn.com/arterialbloodgasanalysis-240926093129-8ee10b45/75/Arterial-Blood-GAS-Analysis-pptx-4-2048.jpg)
![H+
Concentration and HCo3
-
At normal H+
conc. Of 40 nEq./L (pH 7.4), HCo3
-
level is
24 mEq./L, range 22 - 26 meq./L.
• HCo3
-
< 22 meq./L Metabolic acidosis
[Acute diarrhoea, RTA, Addition of lactic acid and
Ketoacids]
• HCo3
-
> 26 meq./L Metabolic Alkalosis
[Persistent vomiting, ↑ RAT loop diuretics]
• HCo3
-
homeostasis is regulated by kidneys by
-](https://image.slidesharecdn.com/arterialbloodgasanalysis-240926093129-8ee10b45/75/Arterial-Blood-GAS-Analysis-pptx-8-2048.jpg)
![Respiratory Alkalosis
• Mild respiratory disorders Hypoxemia
↓
Oxygenation Failure
[Type I Respiratory Failure]
• Hypoxic drive Hyper ventilation
↓
Washing out CO2
↓
Respiratory alkalosis
• Correction of basic pathological condition
+
Prompt O2 supplementation
• Hysterical breathing Rebreathing in paper bag](https://image.slidesharecdn.com/arterialbloodgasanalysis-240926093129-8ee10b45/75/Arterial-Blood-GAS-Analysis-pptx-25-2048.jpg)
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Arterial Blood GAS Analysis.pptx
- 1. Arterial Blood GASAnalysis (ABG) In Pediatric Practice
- 2. Arterial Blood GASAnalysis (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, O2 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 Co2 (Removed by lungs) • Co2 (ventilatory failure) Kidneys as H+
- 6. H+ Concentration & Co2 •Organic compounds Co2 ↓ Removed by alveolar ventilation • Normal PaCo2 40 mm of Hg (Range 36 – 44 mm of Hg) • PaCo2 > 44 mm of Hg Respiratory acidemia (Ventilatory failure) • PaCo2 < 36 mm of Hg Respiratory alkalosis • Paco2 . Sensitive index of alveolar ventilation . Inversely related to alveolar ventilation . Controlled by chemoreceptors in hypothalamus oxidized During intermediary metabolism
- 7. • 95% ofCo2 produced is transported by the RBC and 5% by plasma ↓ 99.9% as physically dissolved (dco2) 0.1% as chemically dissolved (H2 Co3) ↓ The pressure exerted by dco2 PaCo2 ↓ Total Co2 (Tco2) dCo2 + H2Co3. • In RS disturbances, PaCo2 is not affected initially as diffusion capacity of Co2 20 times > O2 • For every 20 mm of Hg ↑ PaCo2 ↓ pH 0.1 • For every 10 mm of Hg ↓ PaCo ↑ pH 0.1
- 8. H+ Concentration and HCo3 - Atnormal H+ conc. Of 40 nEq./L (pH 7.4), HCo3 - level is 24 mEq./L, range 22 - 26 meq./L. • HCo3 - < 22 meq./L Metabolic acidosis [Acute diarrhoea, RTA, Addition of lactic acid and Ketoacids] • HCo3 - > 26 meq./L Metabolic Alkalosis [Persistent vomiting, ↑ RAT loop diuretics] • HCo3 - homeostasis is regulated by kidneys by -
- 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 pHwith Co2 & HCo3 - Henderson - Hasselbalch Equation pH = = ↓ It is the ratio of PCo2 to HCo3 that really decides the pH more than the absolute value. HCo3 - PaCo2 Renal compensation Pulmonary Compensation
- 11. Acid - BaseDisorder • 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 - BaseDisorder • When HCo3 - loss occurs from body (Primary event) ↓ RS comes to rescue eliminating Co2 (compensatory) ↓ till pH N along with buffers (12 – 24 hours) • When Co2 is accumulated in the body (Primary event) ↓ Kidneys retain HCo3 - (compensatory) & along with buffers normalize the pH (3 to 5 days) • Acid Base Disorder may be, - Acute (uncompensated) - Subacute (Partially Compensated)
- 13. Acid - BaseDisorder Stages of Compensation Primary Disturbance pH HCo3 - PCo2 Metabolic acidosis Acute ↓ ↓ N Partially Compensated ↓ ↓ ↓ Fully Compensated N ↓ ↓ Respiratory Acidosis Acute ↓ N ↑ Partially Compensated ↓ ↑ ↑ Fully Compensated N ↑ ↑
- 14. Acid - BaseDisorder Stages of Compensation Primary Disturbance pH HCo3 - PCo2 Respiratory Alkalosis Acute ↑ N ↓ Partially Compensated ↑ ↓ ↓ Fully Compensated N ↓ ↓ Metabolic Alkalosis Acute ↑ ↑ N Partially Compensated ↑ ↑ ↑ Fully Compensated N ↑ ↑
- 15. Metabolic Acidosis • Commonestacid base disorder • Mechanisms: - Loss of HCo3 - (GIT/Kidney) - Addition of acids (LA/KA) - Administration of fluid devoid of HCo3 - (TPN/massive transfusion) • Metabolic acidosis - With ↑ anion gap - With normal anion gap.
- 16. Anion Gap • Accordingto 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- + HCo3 - ) + (Unmeasured anions) (Anion gap) (135 + 04) = (100 + 24) + 8 to 16
- 17. Metabolic Acidosis • Insome types addition of acids ↓ ↓ HCo3 - ↓ ↑ Unmeasured anions without any alteration of Cl- ↓ . Metabolic Acidosis with increased anion gap . Normochloremic acidosis • Loss of HCo3 - ↑ Cl- ↓ Metabolic acidosis with normal anion gap Hyperchloremic acidosis ↓ HCo3 - correction judiciously Administration of HCo3 - may be hazardous
- 18. • Correction ofacidosis should be attempted only when: . HCo3 - < 15 meq./L . pH 7.2 . Base deficit 10 mmol/L • Overzealous correction of acidosis with HCo3 - ↓ (Hypertonic solution ) ∙ Shifting of oxygen - Hb dissociation curve to the left poor O2 release at tissue ∙ Hypokalemia ∙ Hypocalcemic tetany ∙ IVH ∙ Hypernatremia • HCo3 - correction 0.6 * Body wt (kg) * (15 – measured HCo3 - ) ↓ . 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 . DiabetesMellitus . 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 • CaCl2, Mgcl2, NH4 Cl • Small bowel or biliary fistula
- 20. Metabolic Alkalosis Acid loss (a)GIT loss • Vomiting • N – G tube aspiration (b) Mineralo corticoid activity • Cushing’s syndrome • Hyperaldosteronism • Bartter’s syndrome • Liquoric carbenoxolone Alkali gain • Rapid HCo3 - correction • Massive transfusion (citrate) • Excessive antacids ECF loss Cl- > HCo3 - • Cystic fibrosis • Massive Diuresis
- 21. Metabolic Alkalosis Clinical presentation: •Shallow respiration (attempt to conserve Co2) • 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 HCo3 - eliminated • ↓ production of NH3 ↓ Normalizing basic pathology
- 22. Metabolic Alkalosis If ECFvolume is not adequately maintained ↓ Low GFR ↓ HCo3 - 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 • Mildrespiratory disorders Hypoxemia ↓ Oxygenation Failure [Type I Respiratory Failure] • Hypoxic drive Hyper ventilation ↓ Washing out CO2 ↓ Respiratory alkalosis • Correction of basic pathological condition + Prompt O2 supplementation • Hysterical breathing Rebreathing in paper bag
- 26. Respiratory Acidosis Ventilatory TypeII Failure Respiratory (a) Obstructive • Aspiration • Croup • FB • Epiglottitis • Asthma • Bronchiolotis (b) Paranchymal • Pneumonia • RDS • Interstitial lung disease • Pulmonary oedema (c) Pleural • Pleural effusion • Pneumothorax Thoracic Cage . Flail chest . Scoliosis Neuromuscular • Brain stem lesions • Opium • Poliomyelitis • G B syndrome • Myasthenia Gravis • Botulism • Picwickian
- 27. Oxygen Homeostasis • Pao2normal 80 - 100 mm of Hg Newborn 40 – 70 mm of Hg • Hypoxemia: Mild Pao2 60 - 80 mm of HG Moderate Pao2 40 - 60 mm of HG Severe Pao2 < 40 mm of HG • Pao2 O2 level in arterial blood • Adequacy of tissue oxygenation decides cellular metabolism • Delivery of O2 to tissues depends on, - Pao2 - Circulation - Hb - Mitochondrial function Shift of O2 - Hb dissociation curve to right
- 28. Practical Workup ofABG 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 - Co2 tension PaCo2 40 36 – 44 mm of Hg Base Excess BE 0 -2 to 2 mmol/L Total Co2 TCo2 25 23 - 27 mmol/L Actual HCo3 HCo3 24 22 – 26 nmol/L Standard HCo3 SBC 24 22 – 26 mmol/L O2 Saturation SaO2 98 95 – 100 % O2 tension PaO2 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 O2 values & lower Co2 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 bystep Approach I. pH: Acidosis/Alkalosis II. Respiratory/Metabolic III. Stages of compensation IV. Oxygen status V. Simple disorder/Mixed disorder VI. Acute/Chronic VII.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 ↑ PaCo2 / ↓ HCo3 - • Alkalemia due to ↓ PaCo2 / ↑ HCo3 - • In Respiratory Acidosis, Kidney regenerates HCo3 - & ↑ HCo3 - as a compensatory response in addition to hypervantilation
- 32. • Metabolic acidosisis compensated by hyperventilation (Kussmaul’s breathing) elimination of Co2 increases the pH to alkaline side. • Metabolic alkalosis occurs when HCo3 - level exceeds the normal limits, which is compensated by hyperventilation to ↑ Co2 level.
- 33. Step III: Stagesof compensation Acute (Uncompensated stage): pH and PaCo2 / HCo3 - 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 - Co2 & HCo3 - in same direction • Chronic (Fully compensated): - pH Normal - PCo2 & HCo3 - abnormally altered
- 34. Stage IV: Oxygenationstatus • PaO2 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% O2 irrespective of oxygen status O2 supplementation below 60% to avoid O2 toxicity (BPD & RF) • If Hb is inadequate, final delivery of O2 to the tissues will be compromised.
- 35. Stage V: Simple/MixedDisorder • Simple disorder: PaCo2 & HCo3 - change in same direction ↓ Change in trend Mixed disorder • The difference between TCo2 & HCo3 - is > 1.2 in addition to metabolic cause ↓ Underlying respiratory disturbance • Both actual HCo3 - & standard HCo3 - 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 DisorderCompensation Metabolic acidosis: For every 1 meq./L ↓ in HCo3 - , PaCo2 ↓ by 1 mm of Hg (1 – 1.5) Metabolic alkalosis: For every 1 meq./L ↑ in HCo3 - , PaCo2 ↑ by 1 mm of Hg (0.5 – 1) Respiratory acidosis: Acute: For every 1 mm ↑ PaCo2, HCo3 - ↑ by 0.2 meq./L Chronic: For every 1 mm ↑ PaCo2, HCo3 - ↑ by 0.4 meq./L Respiratory alkalosis: Acute: For every 1 mm ↓ PaCo2, HCo3 - ↓ by 0.2 meq./L Chronic: For every 1 mm ↓ PaCo2, HCo3 - ↓ by 0.5 meq./L
- 37. Stage VII: LaboratoryError Henderson Hassel bach equation, H (nmol/L) = 24 (PCo2 / HCo3 - ) ↓ If two are known, third can be calculated ↓ If there is discrepancy between measured value & calculated values ↓ Laboratory Error ?