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Acid and Base Balance

Acid and Base Balance. Dr Sanjay De Bakshi MS;FRCS. USERNAME:- CMRI PASSWORD:- SDB123. INTERPRETATION OF BLOOD GASES. Look at the PaO 2. Is the patient hypoxaemic? What is the A-a gradient {Alveolar - Arterial oxygen difference (A-a)DO 2 }

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Acid and Base Balance

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  1. Acid and Base Balance Dr Sanjay De Bakshi MS;FRCS USERNAME:- CMRI PASSWORD:- SDB123

  2. INTERPRETATION OF BLOOD GASES

  3. Look at the PaO2. Is the patient hypoxaemic? What is the A-a gradient {Alveolar - Arterial oxygen difference (A-a)DO2} (A-a)DO2 = FiO2 x (atmospheric pressure – SVP of water) – PaCO2 – PaO2. (A-a)DO2=(FiO2 x{101-6.2}-PaCO2 -PaO2 INTERPRETING BLOOD GASES APACHE

  4. INTERPRETING BLOOD GASES • Look at the PaCO2. • Look at the pH. Alkalotic or Acidic?

  5. INTERPRETING BLOOD GASES cPaCO2 = pH SBE = pH

  6. Respiratory acidosis • Background: Respiratory acidosis is a clinical disturbance that is due to alveolar hypoventilation. Production of carbon dioxide occurs rapidly, and failure of ventilation promptly increases the partial arterial pressure of carbon dioxide (PaCO2). The reference range for PaCO2 is 36-44. Alveolar hypoventilation leads to an increased PaCO2 (ie, hypercapnia). The increase in PaCO2 in turn decreases the HCO3-/PaCO2 and decreases pH. What are the types of Respiratory Failure?

  7. TYPE I FAILURE HYPOXIC PaO2 < 8kPa NORMAL OR LOW PaCO2 Impaired alveolar function; pneumonia,pulmonary oedema; ARDS TYPE II FAILURE HYPERCAPNIC PaO2 <8kPa PaCO2 > 8kPa Impaired alveolar ventilation; COPD, airway impairment,chest wall deformity, neuromuscular conditions RESPIRATORY FAILURE

  8. Compensation in Respiratory acidosis • In acute respiratory acidosis, compensation occurs in 2 steps. • The initial response is cellular buffering that occurs over minutes to hours. Cellular buffering elevates plasma bicarbonate (HCO3-) only slightly, approximately 1 mEq/L for each 10-mm Hg increase in PaCO2. • In chronic respiratory acidosis, the second step is renal compensation that occurs over 3-5 days. With renal compensation, renal excretion of carbonic acid is increased and bicarbonate reabsorption is increased. In renal compensation, plasma bicarbonate rises 3.5 mEq/L for each increase of 10 mm Hg in PaCO2.

  9. Respiratory acidosis The expected change in serum bicarbonate concentration in respiratory acidosis can be estimated as follows: • Acute respiratory acidosis: HCO3- increases 1 mEq/L for each 10-mm Hg rise in PaCO2. • Chronic respiratory acidosis: HCO3- rises 3.5 mEq/L for each 10-mm Hg rise in PaCO2.

  10. Respiratory alkalosis • Respiratory alkalosis is a clinical disturbance due to alveolar hyperventilation. Alveolar hyperventilation leads to a decreased PaCO2 level (hypocapnia). In turn, the decrease in PaCO2 level increases the ratio of bicarbonate concentration (HCO3-) to PaCO2 and increases the pH level. Hypocapnia develops when the lungs remove more carbon dioxide than is produced in the tissues.

  11. Respiratory alkalosis Respiratory alkalosis can be acute or chronic. • In acute respiratory alkalosis, the PaCO2 level is below the lower limit of normal and the serum level is alkalemic. • In chronic respiratory alkalosis, the PaCO2 level is below the lower limit of normal, but the pH level is normal or near normal because of renal compensation.

  12. Respiratory alkalosis • Acute hyperventilation with hypocapnia causes a small early reduction in serum bicarbonate due to cellular uptake of bicarbonate. Acutely, plasma pH and bicarbonate concentration vary proportionately with the PaCO2 along a range of 15-40 mm Hg. • After a period of 2-6 hours, respiratory alkalosis is compensated by the kidneys by a decrease in bicarbonate reabsorption.

  13. Respiratory alkalosis • The expected change in serum bicarbonate concentration ([HCO3-]) can be estimated as follows: • Acute - [HCO3-] falls 2 mEq/L for each decrease of 10 mm Hg in the PaCO2 (Limit of compensation: [HCO3-] = 12-20 mEq/L) • Chronic - [HCO3-] falls 5 mEq/L for each decrease of 10 mm Hg in the PaCO2 (Limit of compensation: [HCO3-] = 12-20 mEq/L)

  14. CONTROL OF VENTILATION CORTICO-SPINAL TRACT

  15. Regulation of Ventilation • Chemical Control • Non chemical Control ?

  16. REGULATION OF VENTILATION • CHEMICAL CONTROL • CO2 - via CSF H+ CONCENTRATION • O2 - via CAROTID AND AORTIC BODIES • H+ - via CAROTID AND AORTIC BODIES • NON CHEMICAL CONTROL • Afferents from Pons, Hypothalamus & Limbic System. • Afferent from Proprioceptors. • Afferents from pharynx, trachea & bronchi. • Vagal efferents from inflation/ deflation receptors in lung. • Afferents from baroreceptors: arterial, atrial, ventricular & pulmonary.

  17. INTERPRETING BLOOD GASES cPaCO2 = pH SBE = pH

  18. METABOLIC CHANGESACIDOSIS EFFFECTS OF METABOLIC ACIDOSIS • Increased respiratory drive (?){pH <7.1}. • Decreased response to inotropes. • H+ ions into cells and K+ out as buffering action. • Hyperkalaemia.

  19. ANION GAP • The formula (Anion Gap = Na+ - HCO3- - Cl-). • Also important to define the TYPE of metabolic acidosis.

  20. CAUSES OF METABOLIC ACIDOSIS METABOLIC CHANGES Anion Gap = Na+ - (HCO3-+Cl-) Calculating NaHCO3 = ½ x base deficit(mmols/l x weight(kg) 3 Very rarely needed!!!!!

  21. COMPENSATORY MECHANISMS • BLOOD - Buffers. • RESPIRATORY – increased ventilation – CO2 blown off. • KIDNEYS – HCO3 secreted all reabsorbed.

  22. BUFFERS IN BLOOD • Plasma proteins. • Imidazole groups of the histidine residues of haemoglobin. • Carbonic acid bicarbonate system. • Phosphate system (intracellular) Therefore use of bicarbonate only for the pH < 7.2 in an inotrope resistant hypotensive patient

  23. METABOLIC CHANGESALKALOSIS EFFFECTS OF METABOLIC ALKALOSIS • Reduced respiratory drive. • H+ ions out of cells and K+ in as buffering action. • Hypokalaemia. • Hypocalcaemia – tetany, paresthesia

  24. COMPENSATORY MECHANISMS • RESPIRATORY – Reduced respiration = retention of CO2 = increased H+ • RENAL – Increased HCO3 excretion

  25. RELATION BETWEEN BASE EXCESS AND pCO2 • Whenever the pH is normal, i.e., pH = 7.4. then the PCO2 and the SBE are equal and opposite. In such circumstances, if the PCO2 is described as a marked acidosis then logically the SBE must be the exact opposite, a marked alkalosis. • Fortunately, the slope for BE/PCO2 when ph = 7.4 gives us this ratio: three units of change in the SBE is equivalent to a five mmHg change in the PCO2. • Thus, (change in) pCO2: (change in) SBE = 5:3 • Therefore, chpCO2/chSBE=5/3

  26. INTERPRETING BLOOD GASES cPaCO2 = pH SBE = pH

  27. INTERPRETATION OF BLOOD GASES

  28. Example A: pH = 7.2, PCO2 = 60 mmHg, SBE = 0 mEq/L Overall change is acid. Respiratory change is also acid - therefore contributing to the acidosis. SBE is normal - no metabolic compensation. Therefore, pure respiratory acidosis. Typical of acute respiratory depression. Magnitude: marked respiratory acidosis EXAMPLES ?

  29. Example B: pH = 7.35, PCO2 = 60 mmHg, SBE = 7 mEq/L Overall change is slightly acid. Respiratory change is also acid - therefore contributing to the acidosis. Metabolic change is alkaline - therefore compensatory. The respiratory acidosis is 20 mmHg on the acid side of normal (40). To completely balance plus 20 would require 20 X 3 / 5 = 12 mEq/L SBE The actual SBE is 7 eEq/L, which is roughly half way between 0 and 12, i.e., a typical metabolic compensation. The range is about 6mEq/L wide - in this example between about 3 and 9 mEq/L. Magnitude: marked respiratory acidosis with moderate metabolic compensation EXAMPLES ?

  30. Example C: pH = 7.15, PCO2 = 60 mmHg, SBE = -6 mEq/L Overall change is acid. Respiratory change is acid - therefore contributing to the acidosis. Metabolic change is also acid - therefore combined acidosis. The components are pulling in same direction - neither can be compensating for the other Magnitude: marked respiratory acidosis and mild metabolic acidosis EXAMPLES ?

  31. Example D: pH = 7.30, PCO2 = 30 mmHg, SBE = -10 mEq/L Overall change is acid. Respiratory change is alkaline - therefore NOT contributing to the acidosis. Metabolic change is acid - therefore responsible for the acidosis. The components are pulling in opposite directions. SBE is the acid component so it is primarily a metabolic problem with some respiratory compensation The metabolic acidosis is 10 mEq/L on the acid side of normal (0). To completely balance 10 would require 10 * 5 / 3 = 17 mmHg respiratory alkalosis (= 23 mmHg) The actual PCO2 is 30 eEq/L which is roughly half way between 23 and 40, i.e., a typical respiratory compensation. The range is about 10 mmHg wide - in this example between about 27 and 37 mmHg. Magnitude: marked metabolic acidosis with mild respiratory compensation. EXAMPLES ?

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