Acid & base disturbance, ABG Interpretation.pptx

This slide is describe in detail about acid base disturbances and ABG interpretation

1. Acid-Base Disturbance & ABG Interpretation MADAM ROZILA BINTI IBRAHIM MAY SESSION 2024

2. Introduction Disorders of acid-base balance can be found in as many as nine of every 10 patients in the ICU , which means that acid-base disorders may be the most common clinical problems you will encounter in the ICU.

3. Getting an Arterial Blood Gas Sample

4. A change in the normal value of extracellular pH that may result when renal or respiratory function is abnormal or when an acid or base load overwhelms excretory capacity. Normal acid base values                                           pH                   PCO2            HCO3        Range:               7.35- 7.45            36-44            22-26     Optimal value          7.40                   40                 24 Acidemia  - ↓ in the blood pH below normal range Alkalemia  - ↑ in blood pH above the normal range Acid Base Disorder  

5. Disturbance of Acid- Base Balance

6. Mixed Acid-Base Disturbance Occurs when primary respiratory or metabolic disturbance occur simultaneously. If these two processes oppose each other, the pattern will be similar to a compensated acid-base disturbance and the resulting pH derangement will be minimized. But if the two processes cause pH to move in the same direction, a profound acidaemia / alkalaemia may result.

7. Metabolic Acidosis Any process, other than a rise in PaCO 2 that acts to lower pH. It may occur through accumulation of metabolic acid or through excess loss of base. Calculating the anion gap may help to establish the cause of it. It is recognized on an ABG by low HCO 3, & there is a compensatory increase in alveolar ventilation to lower PaCO 2. If compensation is overwhelmed, an academia will result. An HCO 3 < 15mmol/L (@ BE < 10) indicates a severe acidotic, whereas pH <7.25 (H⁺>55) constitutes serious acidaemia .

8. Measuring the Anion Gap To achieve electrochemical balance, the concentration anions must equal the concentration of cations . All ions participate in this balance such as Na⁺, CL⁻, and HCO 3 ⁻ and those that are not measured. Na + UC = (CL + HCO3) + UA Rearranging the terms in this equation yields Anion Gap Na - (CL + HCO3) = UA – UC The difference (UA - UC) is a measure of the relative abundance of unmeasured anions and is called the anion gap (AG) . The normal value of the AG was originally set at 12 ± 4 mEq /L (range = 8 to 16 mEq /L).

9. Normal Anion Gap When a metabolic acidosis is caused by the loss of bicarbonate ions from the extracellular fluid, the bicarbonate loss is counterbalanced by a gain of chloride ions to maintain electrical charge neutrality. Because the increase in chloride concentration is proportional to the decrease in bicarbonate concentration, the relationship AG = Na - (CL + HCO 3 ) remains unchanged. Because normal AG metabolic acidoses are accompanied by increased chloride concentrations, they are often referred to as hyperchloremic metabolic acidoses .

10. High Anion Gap When a fixed acid is added to the extracellular space, the acid dissociates to produce hydrogen ions and anions. The hydrogen ions combine with bicarbonate (HCO 3 ) to form carbonic acid and, according to the relationship AG = Na - (CL + HCO 3 ), the decreased HCO 3 results in an increased AG. The usual causes of an elevated AG metabolic acidosis are lactic acidosis, ketoacidosis, and end-stage renal failure (where hydrogen ion secretion in the distal tubules is impaired). Elevated AG acidosis can also be seen in certain toxic ingestions, including methanol (which forms formic acid), ethylene glycol (which forms oxalic acid), propylene glycol (which accelerates the formation of lactic acid and pyruvic acid), and salicylates (which form salicylic acid).

11. Management of Metabolic Acidosis Treat the underlying cause Restoration of normal tissue perfusion and oxygenation Buffer therapy (NAHCO3) as indicated below: Dose = (weight Kg x base deficit x 0.3) Indication Rationale Severe hypobicarbonatemia (<4 mEq /L) Insufficient buffer concentration may lead to extreme academia with small increase in acidosis Severe acidemia (pH<7.20) with sign of shock/ myocardial irritability & not rapidly respond to tx Therapy for the underlying causes of acidosis depends upon adequate organ perfusion Severe hyperchloremic acidemia Loss bicarb . must be regenerated by kidneys & liver, which may require days

12. Metabolic Alkalosis Any process, other than a fall in PaCO 2 , that acts to increase blood pH and is characterized by rise in plasma HCO 3. Loss of H⁺ may initiate the process but the kidneys have huge scope to correct threatened alkalosis by increasing HCO 3 excretion. The usual suspects are depletion of CL⁻, K⁺ and Na⁺ in most cases due to either sustained vomiting or diuretic drugs. Respiratory compensation (↑ PaCO 2 ) occurs to limit the resulting alkalaemia but is limited by need to avoid hypoxaemia .

13. One source of error occurs in the early stages of diuretic therapy, when the urinary chloride concentration is elevated in a chloride-responsive metabolic alkalosis.

14. Treatment of Metabolic Alkalosis Electrolytes to replace those lost Treat underlying disorder IV chloride containing solution e.g saline Cl Deficit ( mEq ) = 0.2 × Wt (kg) × (Normal Cl- Actual Cl) KCL indicated only for patients who are hypokalemic HCL infusion (0.1 N HCL = 100 mmol /L) reserved for patients with severe alkalemia (pH >7.5), not candidates for saline infusions or potassium replacement, or have failed these therapies 18

15. Respiratory Acidosis A respiratory acidosis is simply, an increase in PaCO 2. Since CO 2 dissolves in blood to form carbonic acid, this has the effect of lowering pH. Normally, lungs are able to increase ventilation to maintain a normal PaCO 2 even in condition of increase CO 2 production ( eg : sepsis). Thus, respiratory acidosis always implies a degree of reduced alveolar ventilation. This may occur from any cause of type 2 respiratory impairment or to counteract a metabolic alkalosis.

16. Treatment of Respiratory Acidosis Restore & improve alveolar ventilation IV lactate solution (converted to bicarbonate ions in the liver). Treat underlying dysfunction or disease ( e.g. pulmonary odema , respiratory depression) 22

17. Respiratory Alkalosis A respiratory alkalosis is decrease in PaCO2, and caused by alveolar hyperventilation. Primary causes include pain, anxiety, fever, breathlessness and hypoxemia. It may also occur to counteract a metabolic acidosis.

18. Treat underlying cause Breathe into a paper bag ???

19. Steps to an Arterial Blood Gas Interpretation

20. IDENTIFY PRIMARY ABNORMALITY Arterial Blood Gas Interpretation Step 1 Assess the pH to determine if the blood is within normal range, alkalotic or acidotic. If it is above 7.45, the blood is alkalotic . If it is below 7.35, the blood is acidotic. Step 2 Compare the pH and the PaCO 2 values. If pH and PaCO 2 are indeed moving in opposite directions, then the problem is primarily respiratory in nature .

21. Step 3 Compare pH and HCO 3 , If they are moving in the same direction, then the problem is primarily metabolic in nature. Step 4 Is there any (if any) compensation occurring? No compensation: pH remains abnormal, and the ‘other’ value (where the problem isn’t occurring, i.e. CO 2 or HCO 3 -) will remain normal or has made no attempt to help normalise the pH. For example: in uncompensated metabolic acidosis: pH 7.23, HCO 3 - 15mmol/L, and the CO 2 will be normal at 40mmHg.

22. . Partial compensation pH is still abnormal, and the ‘other’ value is abnormal in an attempt to help normalise the pH. For example: in partially compensated respiratory alkolosis : pH 7.62, CO 2 27 and the HCO 3 - will be abnormal at 17mmol/L Full compensation The pH is normal, as the ‘other’ value is abnormal and has been successful in normalising the pH. For example: Fully compensated metabolic acidosis pH 7.38, HCO 3 - 15mmol/L and the CO 2 30mmHg

23. In compensated acid-base disorders, the pH will frequently fall either on the low or high side of neutral (7.40).

24. Identify any secondary abnormality Metabolic Acidosis, calculate expected PaCO2 by Winter’s formula : PaCO 2 =1.5 ( HCO₃) + 8 ( ± 2 ) if measured pCO ₂ is lower than expected → concurrent respiratory alkalosis if measured pCO ₂ is higher than expected → concurrent respiratory acidosis

25. . Calculate expected PaCO 2 = (0.6 ( HCO₃ - 24) ) + 40 mmHg if measured pCO ₂ is lower than expected → concurrent respiratory alkalosis if measured pCO ₂ is higher than expected → concurrent respiratory acidosis Metabolic Alkalosis

26. . Acute HCO₃⁻ changes 1-2 for every change in PCO 2 by 10mmHg pH changes 0.08 for every change in PCO 2 by 10mmHg. Chronic HCO₃⁻ changes 4-5 for every change in PCO 2 by 10mmHg, pH changes 0.08 for every change in PCO 2 by 10mmHg. if measured HCO₃⁻ is lower than expected → concurrent metabolic acidosis if measured HCO₃⁻ is higher than expected → concurrent metabolic alkalosis Respiratory Acidosis or Respiratory Alkalosis

27. Oxygenation status Look at the PaO 2 and the %HbO 2 The PaO 2 must always be interpreted in light of the oxygen concentration the patient is receiving. A PaO 2 of 85 mmHg when breathing room air (21%) indicates the lungs are functioning normally but a PaO 2 of 85 when breathing 100% oxygen means the lungs are greatly impaired in their ability to move oxygen into the blood.

28. P A-a O 2 gradient It’s a useful tool in evaluating how well a patient is oxygenating. P A-a O 2= PAO2 – PaO2 = {(760-47) x FiO2 – PaCO2/0.8} – PaO2 Normal = 10-20 mmHg Elevated values is caused by: Parenchymal disease (V/Q mismatch) Diseases of vasculature and shunts: right-to-left shunt, pulmonary embolism interstitial lung diseases: ARDS, pneumonia, emphysema.

29. Respiratory Failure Type 1: defined as hypoxaemia without hypercapnia. P a O 2 low (< 60 mmHg) P a CO 2 normal or low P A-a O 2 increased Type 2: type 2 respiratory failure is characterized by: P a O 2 decreased P a CO 2 increased P A-a O 2 normal pH decreased ABG is used to describe inadequate gas exchange by the respiratory system.

30. Questions All of the following might be a cause of respiratory acidosis except: Sedation Head trauma COPD Hyperventilation pH 7.33 ,PaCO2 60 ,HCO3 34 A. Normal ABG values B. Respiratory acidosis without compensation C. Respiratory acidosis with partial compensation D. Respiratory acidosis with full compensation

31. . pH 7.48 PaCO2 42 HCO3 30 Metabolic acidosis without compensation Respiratory alkalosis with partial compensation Respiratory alkalosis with full compensation Metabolic alkalosis without compensation pH 7.45 PaCO2 26 HCO3 16 Normal Respiratory acidosis fully compensated Respiratory alkalosis fully compensated Metabolic alkalosis fully compensated

32. . pH 7.25 PaCO 2 68 PaO 2 52 B.E. +1 %HBO 2 88% Interpretation ??

33. Patient is brought to ER comatose. Provisional diagnosis is diabetic shock. Room air blood gases: pH 7.16 PaCO 2 18 PaO 2 95 B.E. -12 %HBO 2 98% Interpretation ??

34. You find your patient non-responsive with no sign of breathing or heart rate. The code team arrives and a blood gas is drawn immediately while patient is receiving 100% oxygen. pH 6.98 PaCO 2 86 PaO 2 34 B.E. -12 %HBO 2 74% Interpretation ??

35. References Ellstrom , K. (2006). The Pulmonary System. In J. G. Alspach , Core Curriculum for Critical care Nursing (pp. 62-68). United State of America: Saunders Elsevier. Hennessey, L. A., & Japp , A. G. (2007). Arterial Blood Gases Made Easy. China: Elsevier. Hinds, C., & Watson, D. (2008). Intensive Care: A Concise Textbook (Vol. III). Great Britain: Elsevier. Nicolaou , D. D., & Kelen , G. D. (2011). Acid-Base Disorder. In J. E. Tintinalli , J. S. Stapczynski , D. M. Cline, O. John Ma, R. K. Cydulka , & G. D. Meckler, Tintinalli's Emergency Medicine: A Comprehensive Study Guide (pp. 102-116). China: McGraw-Hill.