Approach to Acid-Base Disorders

1. Approach to Acid-Base Disorders Antonio Renato B. Herradura, M.D. F.P.C.P, F.P.C.C.P UERMMMC

2. Importance of Acid-Base Disorders • Among the most common clinical problems encountered in hospitalized patients, especially ICU patients • Lead to significant physiologic effects • Proper management may be life-saving

3. Acid – Base Disorders • Principles of A-B homeostasis and disturbances • Recognition of A-B disorders • Specific disorders: common etiologies, pathogenesis, clinical features, general principles of management • Interpretation of ABG and electrolyte results

4. Normal Arterial Blood Values • pH: 7.35 - 7.45 • pCO2: 35 - 45 mmHg • HCO3: 22 – 26 mmol/L • pO2, O2 saturation, base excess/deficit

5. Normal Arterial Blood Values • pH: 7.35 - 7.45 • pCO2: 35 - 45 mmHg • HCO3: 22 – 26 mmol/L • pO2, O2 saturation, base excess/deficit • Chemistry panel: • Sodium: 135 - 145 mmol/L Potassium: 3.5 - 5 mmol/L • Chloride: 96 – 109 mmol/L Total CO2: 23 -30 mmol/L • Glucose, BUN, Creatinine

6. Maintenance of blood pH pH = 6.1 + log [HCO3] (pCO2)(0.0301)

7. Maintenance of blood pH pH = 6.1 + log [HCO3] (pCO2)(0.0301) pH α [HCO3] pCO2 pH α [HCO3] pH 1/α pCO2

8. Regulation of pCO2 CO2 production ≈ pCO2 elimination glucose metabolism ventilatory forces neural drive bellows apparatus airways

9. Regulation of plasma HCO3- • Via kidneys: • Reabsorption of filtered HCO3 • Formation of titratable acid • Excretion of NH4+ in urine

10. Maintenance of blood pH • Maintenance of the ratio of HCO3 to pCO2 via compensatory responses by the kidneys and lungs

11. Maintenance of blood pH • Maintenance of the ratio of HCO3 to pCO2 via compensatory responses by the kidneys and lungs • Chemical buffering: • includes HCO3, phosphates, proteins, hemoglobin, bone carbamates

12. Compensation for Acid – Base Disorders Primary metabolic Compensatory disturbance respiratory response HCO3 pH (met. acidosis) pCO2 HCO3 pH (met. alkalosis) pCO2

13. Compensation for Acid – Base Disorders Primary respiratory Compensatory disturbance metabolic response pCO2 pH (resp. alkalosis) HCO3 pCO2 pH (resp. acidosis) HCO3

14. Prediction of Compensatory Responses on Simple Acid - Base Disorders

15. Acid–Base Nomogram

16. Anion Gap • AG = Na+ - (Cl- + HCO3) • Normal: 10 - 14 • e.g. AG = 140 - (105 + 24) = 140 – 129 = 11 • Represents those unmeasured anions in the plasma • Increase in AG is due to increased in the amount of unmeasured anions, and less commonly due to a decrease in unmeasured cations

17. Determinants of AG Unmeasured AnionsUnmeasured Cations Albumin (15mEq/L) Calcium (5 mEq/L) Organic Acids (5 mEq/L) Potassium (4.5 mEq/L) Phosphate (2 mEq/L) Magnesium (1.5 mEq/L) Sulfate (1 mEq/L) ---------------------------- --------------------------- Total UA (23 mEq/L) Total UC (11 mEq/L) AG = UA – UC = 12 mEq/L

18. Metabolic Acidosis PATHOGENESIS • May be due to: • Increased endogenous acid production (e.g. lactate and ketones) • Loss of bicarbonate (e.g. diarrhea) • Decreased excretion of endogenous acids (e.g. renal failure)

19. Common Causes of Metabolic Acidosis HIGH ANION GAP NORMAL ANION GAP Lactic Acidosis Diarrhea Ketoacidosis Isotonic saline infusion ESRD Early renal insufficiency Methanol ingestion RTA Ethylene glycol ingestion Acetazoleamide Salicylate toxicity Ureteroenterostomy

20. Metabolic Acidosis CLINICAL EFFECTS • Kussmaul breathing, dyspnea • Headache, nausea, vomiting, confusion, stupor, coma • Decreased myocardial contractility and response to catecholamine; peripheral vasodilatation with central venoconstriction predisposing to pulmonary edema; arrhythmias

21. Metabolic Acidosis MANAGEMENT • Identify and treat underlying cause. • Give alkali therapy (oral or i.v.) to patients with normal AG acidosis, mixed hyperchloremic and AG acidosis, and AG acidosis due to nonmetabolizable anion in the face of renal failure. • Give modest quantities of i.v. alkali in patients with pure AG acidosis due to metabolizable organic acid anion • Goal: increase pH to 7.15 or [HCO3] to 10 mEq/L

22. Metabolic Alkalosis PATHOGENESIS • Due to net gain of HCO3 or loss of volatile acid (usually HCl by vomiting) • 2 stages: • GENERATIVE STAGE: loss of acid • MAINTENANCE STAGE: failure of kidneys to compensation by excreting HCO3, because of volume contraction, low GFR, or depleted K+ or Cl-

23. Metabolic Alkalosis CLINICAL EFFECTS • increases the affinity of hemoglobin for oxygen ----- decrease tissue unloading • Decreases ventilation • Decreases ionized calcium ----- neuromuscular hyperirritability • Supraventricular and ventricular arrhythmias

24. Metabolic Alkalosis MANAGEMENT • Identify and correct the underlying stimulus for HCO3 generation • Remove the factors that sustain HCO3 reabsorption (e.g. ECF contraction or hypoK+) • Acetazoleamide • Dilute 0.1N HCl or NH4Cl • Hemodialysis

25. Respiratory Acidosis ETIOLOGY and PATHOGENESIS • may be due to severe pulmonary disease (e.g. advanced COPD), respiratory muscle fatigue, or abnormalities in ventilatory control (e.g. stroke)

26. Respiratory Acidosis CLINICAL EFFECTS • depends on severity and acuteness • may be dyspneic or tachypneic • Systemic vasodilation especially cerebral vasodilation ----- increased ICP ----- pseudotumor cerebri • Myoclonic jerks, asterixis, tremors, restlessness, coma

27. Respiratory Acidosis MANAGEMENT • Depends on severity and rate of onset • May be life-threatening • Measures to reverse underlying cause • Restoration of adequate alveolar ventilation • Avoid rapid correction of hypercapnea

28. Respiratory Alkalosis ETIOLOGY and PATHOGENESIS • Develops when a sufficiently strong ventilatory stimulus causes CO2 output in the lungs to exceed its metabolic production in the tissues • May be due to stimulation of CNS (e.g. pain, anxiety), peripheral chemoreceptors (e.g. hypoxemia 2o to pneumonia), chest receptors (e.g. PTE).

29. Respiratory Alkalosis CLINICAL EFFECTS • Panic, weakness, and sense of impending doom • Paresthesias about the hands and feet • Trousseau’s and Chvostek’s signs • Possible tetany, seizures

30. Respiratory Alkalosis MANAGEMENT • Directed toward alleviation of underlying disorder • Change in dead space, tidal volume and respiratory frequency, if on MV • Re-breathing from paper bag during symptomatic attacks of hyperventilation syndrome

31. Interpretation of Acid - Base Disorders • Determine if sample is arterial or venous. • Compare HCO3 on ABG and electrolyte panel to verify accuracy • Determine if pH or pCO2 are normal or abnormal. • If any of above are abnormal determine primary A-B disturbance • Compute for expected compensation to determine presence of mixed disorders.

32. Calculate the Anion Gap RULE: If AG > 20 high AG metabolic acidosis is present regardless of the pH or HCO3. Compare the change in AG (ΔAG) with change in HCO3 (ΔHCO3). RULE: If change (i.e. increase) in AG is < change( i.e. drop) in HCO3, there is combined high AG met acidosis and normal AG (hyperchloremic) acidosis. RULE: If ΔAG is > ΔHCO3, there is combined high AG metabolic acidosis and metabolic alkalosis. Interpretation of Acid - Base Disorders

33. Thank you for your attention! Have a nice day!