1. METABOLIC ACIDOSIS D8

2. HISTORY 45 year old Diabetic woman 4 th day Fever (39.5  C) Chills Myalgia Diarrhea Denies taking any medications, drugs or alcohol

3. PHYSICAL EXAMINATION BP: 84/52 (Supine) PR: 118 bpm RR: 42 breaths/ minute Dry mucous membrane Flat neck veins No edema Abdomen distended, firm & mildly tender Hyperactive bowel sounds

4. LABORATORY CBC ResultReference range Remarks Hemoglobin15.5 g/dL12-16Normal Hematocrit48%38-48%Normal WBC count22,8005,000- 10,000 Normal Segmenters66%50-70%Normal Band forms23%0-5%Increased

5. LABORATORY CHEMISTRY ResultReference range Remark Serum Na138.0 meq/L 135-145Normal Serum Cl108.0 meq/L 99-110Normal Serum K4.2 meq/L4-4.5Normal

6. LABORATORY CHEMISTRY ResultReference range Remark pH7.397.35-7.45Normal pCO217.0 mmHg35-45Decreased HCO310.0 meq/L21-28Decreased

7. LABORATORY CHEMISTRY ResultReference range Remark BUN28.0 mg/dL7-20Increased Creatinine2.4 mg/dL0-8-1.4Increased

8. LABORATORY CHEMISTRY ResultReference range Remark Glucose342.0 mg/dL <100Increased Lactate3.0 meq/L0.5-1.0Increased KetonesNoneNegativeNormal

9. INTRODUCTION Blood pH 7.35 – 7.45 Extracellular & intracellular buffering process Respiratory & renal regulatory mechanisms Dispose the body’s normal physiologic load of carbonic acid (as carbon dioxide), non-volatile acids & defend against occasional addition of abnormal quantities of acids & alkalis

10. BODY SOURCES Volatile acid Carbon dioxide Aerobic metabolism Non-volatile acid From breakdown of protein & phospholipid metabolism Ketoacids, lactic acid, from disease & anaerobic metabolism

11. HYDROGEN REGULATION Chemical buffering Extracellular & intracellular buffers Acts within a fraction of second Respiratory regulation Altering rate of breathing affecting rate of CO 2 removal Acts with minutes to days Renal regulation Excreting either acid or alkaline urine Acts within hours to several days

12. QUESTION 1 What is the acid base disturbance present in this case?

13. What is the acid-base disturbance present in this case? Metabolic Acidosis Metabolic Alkalosis Respiratory Acidosis Respiratory Alkalosis pH H+ PCO2 HCO3-

14. Arterial blood sample pH < 7.40 HCO3 < 24 Metabolic acidosis pCO2 < 40 pCO2 > 40 Respiratory acidosis HCO3 > 24 pH > 7.40 HCO3 >24 Metabolic alkalosis pCO2 > 40 pCO2 < 40 Respiratory alkalosis HCO3 < 24

15. DisturbancePrimary alterationDefense mechanism Metabolic alkalosis plasma [HCO 3 - ]Intracellular buffers Hypoventilation to increase PCO 2  Urinary excretion of HCO 3 - Respiratory acidosis  blood pCO 2 Intracellular buffers Increased renal acid excretion Respiratory alkalosis  blood pCO 2 Intracellular buffers  renal acid excretion Metabolic acidosis  in plasma [HCO 3 ] Intracellular & extracellular buffer Hyperventilation to  pCO 2  Urinary excretion of H +

16. Metabolic Acidosis Metabolic Alkalosis Respiratory Acidosis Respiratory Alkalosis Hx: hypercapnia, dyspnea, anxiety, delirium, obtundation Hx: dizziness, mental confusion, seizures, tetany Hx: palpitations, chest pain, visual changes, mental confusion, dyspnea, n/v, diarrhea, tachypnea, hyperpnea Hx: weakness, myalgia, polyuria, vomitting, diarrhea, hypoventilation

17. METABOLIC ACIDOSIS Addition of non-volatile acids Loss of non-volatile alkali (Diarrhea) Failure to excrete sufficient net acid load

18. COMPENSATION ICF & ECF Buffers Respiratory Renal

19. RESPIRATORY COMPENSATION METABOLIC ACIDOSIS STIMULATE CENTRAL & PERIPHERAL CHEMORECEPTORS INCREASED ALVEOLAR VENTILATION FALL OF pCO2 RAISE pH TOWARD NORMAL

20. QUESTION 2 Present an algorithm for the diagnosis of the acid base disorder. Present the table: rule of thumb in bedside interpretation of acid base disorder

21. STEPS IN ACID-BASE DIAGNOSIS 1.Obtain arterial blood gases (ABGs) and electrolytes (lytes) simultaneously. 2.Compare [HCO3] on ABG and lytes to verify accuracy. 3.Calculate anion gap (AG). 4.Know four causes of high AG acidosis (ketoacidosis, lactic acid acidosis, renal failure and toxins). 5.Know two causes of high hyperchloremic or nongap acidosis (bicarbonate loss from GI tract, renal tubular acidosis). 6.Estimate compensatory response. 7.Compare ΔAG and Δ HCO3 8.Compare change in [Cl] with changes in [Na].

22. STEPS IN ACID-BASE DIAGNOSIS 1.Obtain arterial blood gases (ABGs) and electrolytes (lytes) simultaneously. 2.Compare [HCO3] on ABG and lytes to verify accuracy. * ± 2mmol/L 3.Calculate anion gap (AG). 4.Know four causes of high AG acidosis (ketoacidosis, lactic acid acidosis, renal failure and toxins). 5.Know two causes of high hyperchloremic or nongap acidosis (bicarbonate loss from GI tract, renal tubular acidosis). 6.Estimate compensatory response. 7.Compare ΔAG and Δ HCO3 8.Compare change in [Cl] with changes in [Na].

23. STEPS IN ACID-BASE DIAGNOSIS 1.Obtain arterial blood gases (ABGs) and electrolytes (lytes) simultaneously. 2.Compare [HCO3] on ABG and lytes to verify accuracy. 3.Calculate anion gap (AG). 4.Know four causes of high AG acidosis (ketoacidosis, lactic acid acidosis, renal failure and toxins). 5.Know two causes of high hyperchloremic or nongap acidosis (bicarbonate loss from GI tract, renal tubular acidosis). 6.Estimate compensatory response. 7.Compare ΔAG and Δ HCO3 8.Compare change in [Cl] with changes in [Na].

24. STEPS IN ACID-BASE DIAGNOSIS 1.Obtain arterial blood gases (ABGs) and electrolytes (lytes) simultaneously. 2.Compare [HCO3] on ABG and lytes to verify accuracy. 3.Calculate anion gap (AG). 4.Know four causes of high AG acidosis (ketoacidosis, lactic acid acidosis, renal failure and toxins). 5.Know two causes of high hyperchloremic or nongap acidosis (bicarbonate loss from GI tract, renal tubular acidosis). 6.Estimate compensatory response. 7.Compare ΔAG and Δ HCO3 8.Compare change in [Cl] with changes in [Na].

25. STEPS IN ACID-BASE DIAGNOSIS 1.Obtain arterial blood gases (ABGs) and electrolytes (lytes) simultaneously. 2.Compare [HCO3] on ABG and lytes to verify accuracy. 3.Calculate anion gap (AG). 4.Know four causes of high AG acidosis (ketoacidosis, lactic acid acidosis, renal failure and toxins). 5.Know two causes of high hyperchloremic or nongap acidosis(bicarbonate loss from GI tract, renal tubular acidosis). 6.Estimate compensatory response. 7.Compare ΔAG and Δ HCO3 8.Compare change in [Cl] with changes in [Na].

26. STEPS IN ACID-BASE DIAGNOSIS 1.Obtain arterial blood gases (ABGs) and electrolytes (lytes) simultaneously. 2.Compare [HCO3] on ABG and lytes to verify accuracy. 3.Calculate anion gap (AG). 4.Know four causes of high AG acidosis (ketoacidosis, lactic acid acidosis, renal failure and toxins). 5.Know two causes of high hyperchloremic or nongap acidosis (bicarbonate loss from GI tract, renal tubular acidosis). 6.Estimate compensatory response. 7.Compare ΔAG and Δ HCO3 8.Compare change in [Cl] with changes in [Na].

27. Prediction of Compensatory Responses on Simple Acid Base Disturbances Metabolic Acidosis PaCO2 = (1.5 x HCO) + 8 or PaCO2 will  1.25 mmHg per mmol/L  in HCO3 Metabolic Alkalosis PaCO2 will  0.75 mmHg per mmol/L  in HCO3 or PaCO2 = HCO3 + 15 Respiratory Alkalosis HCO3 will  2-4 most per 10 mmHg  in PaCO2 Respiratory Acidosis HCO3 will  1-4 mmol/L per 10 mmHg  in PaCO2

28. Prediction of Compensatory Responses on Simple Acid Base Disturbances Metabolic acidosis  pH,  HCO3 Stimulate medullary chemoreceptors to  ventilation Predict the degree of respiratory compensation: PaCO2 = (1.5 x HCO3) + 8 = 23 *21-25 mmHg Values 25  mixed disturbance PaCO2 < 23 = met acidosis & respi alkalosis PaCO2 > 23 = met alkalosis & respi acidosis

29. Prediction of Compensatory Responses on Simple Acid Base Disturbances Acid-Base Nomogram Shaded areas show 95% confidence limits for normal compensation Finding acid-base values within the shaded areas does not rule out a mixed disturbance Not a substitute for computation

30. Prediction of Compensatory Responses on Simple Acid Base Disturbances Acid-Base Nomogram pH 7.39 HCO3 10 mEq/L PCO2 17 mmHg

31. STEPS IN ACID-BASE DIAGNOSIS 1.Obtain arterial blood gases (ABGs) and electrolytes (lytes) simultaneously. 2.Compare [HCO3] on ABG and lytes to verify accuracy. 3.Calculate anion gap (AG). 4.Know four causes of high AG acidosis (ketoacidosis, lactic acid acidosis, renal failure and toxins). 5.Know two causes of high hyperchloremic or nongap acidosis (bicarbonate loss from GI tract, renal tubular acidosis). 6.Estimate compensatory response. 7.Compare ΔAG and Δ HCO3 8.Compare change in [Cl] with changes in [Na].

32. STEPS IN ACID-BASE DIAGNOSIS 1.Obtain arterial blood gases (ABGs) and electrolytes (lytes) simultaneously. 2.Compare [HCO3] on ABG and lytes to verify accuracy. 3.Calculate anion gap (AG). 4.Know four causes of high AG acidosis (ketoacidosis, lactic acid acidosis, renal failure and toxins). 5.Know two causes of high hyperchloremic or nongap acidosis (bicarbonate loss from GI tract, renal tubular acidosis). 6.Estimate compensatory response. 7.Compare ΔAG and Δ HCO3 8.Compare change in [Cl] with changes in [Na].

33. QUESTION 3 How do you compute for the anion gap? What is its significance? Compute for the anion gap.

34. ANION GAP Represents the difference in concentration between the major plasma cations & the major plasma anions Cations: Na + Anions: Cl - & HCO 3 -

35. COMPUTING THE ANION GAP Anion Gap = [Na + ] – ([Cl - ] + [HCO 3 - ]) Normal range: 8-16 mEq/L

36. SIGNIFICANCE OF ANION GAP It is a useful way to determine the cause of metabolic acidosis because changes in the concentration of anions are a result of addition of nonvolatile acids. Because the condition is diagnosed as metabolic acidosis, nonvolatile acids are added into the body fluids.

37. ANION GAP If the nonvolatile acid contains Cl - the anion gap will remain normal (because the decrease in HCO 3 - is matched by the increase in Cl - ) If the nonvolatile acid contains another substance, the anion gap will increase (because the Cl - concentration remains unchanged)

38. COMPUTATION OF ANION GAP Anion Gap = [Na + ] – ([Cl - ] + [HCO 3 - ]) Anion Gap = [138.0] – ([108.0] + [10.0]) Anion Gap = (138.0) – (118.0) Anion Gap = 20.0 mEq/L NR: 8-16 mEq/L ** The anion gap is increased

39. QUESTION 4 What are the causes of high anion gap and normal anion gap acidosis?

40. NOMAL VS HIGH NORMAL ANION GAP Acid gain or bicarbonate loss is accompanied by chloride gain Anion gap remains unchanged HIGH ANION GAP Accumulation of acid anions in ECF Exogenous acid ingestion Increased endogenous acid production

41. DIARRHEA ↑ loss of HCO3 along w/ vol. depletion Matabolic acidosis and hypokalemia ↑renal synthesis and excretion of NH4 NORMAL ANION GAP

42. RENAL TUBULAR ACIDOSIS (GFR bet. 20 and 50 mL/min) ↓ # of functioning nephrons Proximal RTA: ↓ HCO3 tubular reabsorption OR Distal RTA: ↓ acid excreation ↑renal synthesis and excretion of NH4

43. OTHER CAUSES OF NORMAL ANION GAP Carbonic anhydrase inhibition Drug-induced hyperkalemia (With renal insufficiency)

44. HIGH ANION GAP Lactic Acidosis Increase in plasma lactate Secondary to poor tissue perfusion (Type A) Aerobic disorders (Type B) Ketoacidosis Increase fatty acid metabolism Accumulation of ketoacids (Acetoacetate &  - hydroxybutyrate) Diabetic ketoacidosis, alcoholic ketoacidosis

45. ↑ ANION GAP Drug and toxin induced Salicylates: ketones, lactate, salicylate ethylene glycol: glycolate, oxalate Methanol or formaldehyde: Formate Advanced Renal failure: Sulfate, phosphate, urate

46. ↑ ANION GAP Advanced RF ↓ # of functioning nephrons Dec. NH4+ prod. and excretion Failure to balance w/ net acid production Inc. anion gap

47. QUESTION 5 How would you treat this patient?

48. Normal AG acidosis (hyperchloremic acidosis), a slightly elevated AG (mixed hyperchloremic and AG acidosis), or an AG attributable to a nonmetabolizable anion in the face of renal failure: --> Alkali theraphy orally (NaHCO3) or Shohl's solution) IV (NaHCO3), in an amount necesarry to slowly increase the plasma [HCO3-] into the 20 to 22 mmol/L range. The condition that precipitated the metabolic acidosis in the patient should also be managed. (Fever and diarrhea ~ Gastroenteritis??)

49. THANK YOU..