Acid Base Management Part -1 .

Human body is made up primarily of water.
Water is slightly ionized into negatively charged (OH-) and positively charged (H+).
Molecules containing hydrogen atoms that can release hydrogen ions in a solution are referred to as acids.
A base is an ion or a molecule that can accept an H+.
The body’s balance between acidity and alkalinity is referred to as acid-base balance.

1. Acid Base Management Part -1 Presenter : Dr. Rakshitha Moderator : Dr. Saraswathi ma’am

2. Introduction Human body is made up primarily of water. Water is slightly ionized into negatively charged (OH-) and positively charged (H+). Molecules containing hydrogen atoms that can release hydrogen ions in a solution are referred to as acids . A base is an ion or a molecule that can accept an H+. The body’s balance between acidity and alkalinity is referred to as acid-base balance.

3. Buffer system of body Three primary systems regulate the H+ concentration in the body fluids : 1. The chemical acid–base buffer systems of the body fluids- which immediately combine with an acid or a base to prevent excessive changes in H+ concentration. 2. The respiratory center - which regulates the removal of CO2 ( therefore H2CO3 ) from the extracellular fluid. 3. The kidneys - excrete acidic or alkaline urine, thereby readjusting the extracellular fluid H+ concentration.

4. Body buffer system

5. 1. The bicarbonate buffer system : H2CO3 is formed in the body by the reaction of CO2 with H2O. Carbonic anhydrase is present abundant in the walls of the lung alveoli, where CO2 is released. Carbonic anhydrase is also present in the epithelial cells of the renal tubules, where CO2 reacts with H2O to form H2CO3.

6. H2CO3 ionizes weakly to form small amounts of H+ and HCO3− Because of the weak dissociation of H2CO3, the H+ concentration is extremely low . When a strong acid is added to the bicarbonate buffer solution, the increased H+ released from the acid is buffered by HCO3 − As a result, more H2CO3 is formed, causing increased CO2 and H2O production

7. 2. Phosphate buffer system : The main elements of the phosphate buffer system are H2PO4 − and HPO4 =. When a strong acid is added to a mixture of these two substances, the hydrogen is accepted by the base HPO4= and converted to H2PO4 −, the decrease in pH is minimized. When a strong base, is added to the buffer system, the OH− is buffered by the H2PO4− to form additional amounts of HPO4= + H2O, causing only a slight increase in pH.

8. 3. Proteins : Approximately 60% to 70% of the total chemical buffering of the body fluids is inside the cells, and most of this buffering results from the intracellular proteins.

9. RESPIRATORY REGULATION OF ACID–BASE BALANCE The second line of defense against acid–base disturbances is control of extracellular fluid CO2 concentration by the lungs. An increase in ventilation eliminates CO2 from extracellular fluid, which by mass action, reduces the H+ concentration. Decrease ventilation increases CO2 and H+ concentrations in the extracellular fluid .

10. RENAL CONTROL OF ACID–BASE BALANCE Renal response to acidemia : Increase reabsorption of filtered HCO3 Increase excretion of titratable acids Increase production of ammonia

11. Increase reabsorption of bicarbonate

12. Increase excretion of titratable acids

13. Increase formation of ammonia

14. Arterial blood gas analysis It is the diagnostic procedure in which a blood is obtained from an artery directly by an artery puncture or accessed by a way of indwelling arterial catheter.

15. Sites for obtaining ABG Radial artery Brachial artery Femoral artery Radial artery is most preferable: Easy to assess It is not deep artery which facilitate palpation, stabilisation and puncturing. The artery has collateral circulation.

16. ALLEN’S TEST It is a test done to determine that the collateral circulation is present from the ulnar artery in case thrombosis occur in the radial artery.

17. Complications: Arteriospasm Hematoma Hemorrhage Distal ischemia Infection

18. ABG component pH: Measures hydrogen ion concentration in the blood .

19. Calculation of pH

20. PaO2: It is the partial pressure of O2 that is dissolved in the blood. Normal PaO2 – 95-100 mm Hg. Mild hypoxemia : 60-80 mm Hg. Moderate hypoxemia : 40-60 mm Hg. Severe hypoxemia : <40 mm Hg.

21. PaCO2: It is the partial pressure of CO2 that is carried by the blood for excretion by the lung. Normal PaCO2 : 35-45mm Hg. HCO3-: Known as metabolic parameter , it reflects the kidney‘s ability to retain and excrete bicarbonate. Normal HCO3 : 22-28meq/l

22. Technical errors Air bubbles : In air bubble PaO2- 150mm Hg and PCO2 is 0mm hg. Mixing sample with air bubble lead to increase in PaO 2 and decrease in PCO2.

23. 2. Excessive heparin : Dilutional effect. Causes decrease in HCO3- and PaCO2. Only 0.05ml heparin is required for 1 ml of blood.

24. 3. Effect of temperature

25. Classification of Acid-Base Disorders The [H +] in extracellular fluid is determined by the balance between the partial pressure of carbon dioxide (PCO2) and the concentration of bicarbonate (HCO3) in the fluid . The PCO2/HCO3 ratio identifies the primary acid-base disorders and secondary responses.

26. Secondary responses The response to a metabolic acid-base disorder involves a change in minute ventilation that is mediated by peripheral chemoreceptors located in the carotid body at the carotid bifurcation in the neck.

27. 1. Metabolic Acidosis : The secondary response to metabolic acidosis is an increase in minute ventilation (tidal volume and respiratory rate) and a subsequent decrease in PaCO2. This response appears in 30–120 minutes, and can take 12 to 24 hours to complete. The magnitude of the response is defined by

28. 2. Metabolic Alkalosis : The secondary response to metabolic alkalosis is a decrease in minute ventilation and a subsequent increase in PaCO2. The magnitude of the response to metabolic alkalosis is defined by

29. Responses to Respiratory Acid-Base Disorders The secondary response to changes in PaCO2 occurs in the kidneys, where HCO3 absorption in the proximal tubes is adjusted to produce the appropriate change in plasma HCO3 . This renal response is relatively slow and can take 2 or 3 days to reach completion. Because of the delay in the secondary response, respiratory acid-base disorders are separated into acute and chronic disorders.

30. STEPWISE APPROACH TO ACID-BASE ANALYSIS Stage I: Identify the Primary Acid-Base Disorder The PaCO2 and pH are used to identify the primary acid base disorder . Rule 1: If the PaCO2 and/or the pH is not within the normal range, there is an acid-base disorder . Rule 2: If the PaCO2 and pH are both abnormal, compare the directional change. 2a. If the PaCO2 and pH change in the same direction , there is a primary metabolic acid-base disorder. 2b. If the PaCO2 and pH change in opposite directions, there is a primary respiratory acid-base disorder.

31. Rule3: If only the pH or PaCO2 is abnormal, the condition is a mixed metabolic and respiratory disorder 3a. If the PaCO2 is abnormal, the directional change in PaCO2 identifies the type of respiratory disorder (e.g., high PaCO2 indicates a respiratory acidosis), and the opposing metabolic disorder. 3b. If the pH is abnormal, the directional change in pH identifies the type of metabolic disorder (e.g., low pH indicates a metabolic acidosis) and the opposing respiratory disorder .

32. Stage II: Evaluate the Secondary Responses Rule 4: For a primary metabolic disorder, if the measured PaCO2 is higher than expected, there is a secondary respiratory acidosis. If the measured PaCO2 is less than expected , there is a secondary respiratory alkalosis. Rule 5: For a primary respiratory disorder, a normal or near-normal HCO3 indicates that the disorder is acute.

33. Rule 6: For a primary respiratory disorder where the HCO3 is abnormal, determine the expected HCO3 for a chronic respiratory disorder . 6a. For a chronic respiratory acidosis, if the HCO3 is lower than expected, there is an incomplete renal response, and if the HCO3 is higher than expected, there is a secondary metabolic alkalosis . 6b. For a chronic respiratory alkalosis, if the HCO3 is higher than expected, there is anincomplete renal response, and if the HCO3 is lower than expected, there is a secondary metabolic acidosis.

34. Stage III: Use The Gaps to Evaluate a Metabolic Acidosis 1. The Anion Gap: The anion gap estimate the relative abundance of unmeasured anions It is used to determine if a metabolic acidosis is due to an accumulation of non-volatile acids or a primary loss of bicarbonate Range for the Anion Gap is 12±4 mEq /L.

35. 2. Delta anion Gap: Determines the presence of other metabolic disturbances superimposed on known anion gap acidosis. It is based on the principle that change in anion gap should approximate to the change in serum bicarbonate in a simple anion acidosis.

36. Metabolic acidosis It is a primary acid base disorder characterized by fall in both pH in blood and bicarbonate level in the plasma.

37. High anion gap metabolic acidosis

38. Normal anion gap metabolic acidosis

39. Clinical features: RS – hyperventilation, Kussmaul’s breathing CVS – decrease myocardial contractility, sympathetic overactivity , CNS – lethargy, disorientation, stupor, coma. Others – hyperkalemia .

40. Respiratory acidosis It is a primary acid-base disorder characterized by increase in PCO2 and decrease in pH.

41. Causes of respiratory acidosis

42. Clinical features : RS- stimulation of ventilation ( tachypnea ) CVS – tachycardia, bounding pulse. CNS – increase cerebral blood flow -> increase ICP, papilledema . - CO2 narcosis – disorientation, confusion, headache. - Coma Others – peripheral vasodilatation.

43. Treatment : Bronchodilators – to treat obstructive airway disease and severe bronchospasm Oxygen therapy. Ventilatory support

44. References Guyton and Hall textbook of Medical Physiology. Paul Marino’s The ICU Book The Washington Manual of Critical care

45. Thank you