Acidosis Metabolic in CVCU [Autosaved].pptx

Acidosis Metabolic in CVCU [Autosaved].pptx

1. How to Deal with METABOLIC ACIDOSIS in CVCU and the role of Mechanical Ventilation Firandi Saputra

2. Definition of Metabolic Acidosis Pathologic process that, when unopposed, increases the concentration of hydrogen ions in the body and reduces the HCO concentration

3. Mechanism

4. Metabolic Acidosis

5. Compensation of Metabolic Acidosis Renal System Respiratory System Buffer system 5

6. Buffer System Extracellular buffering to an acid load is complete within 30 min. Subsequent buffering occurs intracellularly and takes several hours to complete The bone becomes an important source of buffering acid load acutely by an uptake of H+ in exchange for Na+, K+, and bone minerals Hasan, A. (2013).  Handbook of Blood Gas/Acid-Base Interpretation .

7. Compensation of Metabolic Acidosis Hasan, A. (2013).  Handbook of Blood Gas/Acid-Base Interpretation . Reabsorption of HCO3- Acid titration in urine Ammonium generation

8. Clinical Scenario where BGA is useful

9. Identifying Metabolic Acidosis pH <7.38 AND HCO3<20 mmol/L Looking at Bicarbonate level alone isn’t ENOUGH Decrease of bicarbonate  may represent compensatory of respiratory alkalosis CLUE: pH>7.40 and PaCO2<38 mmHg May also mixed acid base  pH may be low, normal, or high  Look at expected respiratory compensation!!

10. Does the use of a diagnostic algorithm improve etiological diagnosis of metabolic acidosis? Experts suggest using an algorithm to improve the etiological diagnosis of metabolic acidosis (EXPERT OPINION) Jung, B., Martinez, M., Claessens , YE.  et al.  Diagnosis and management of metabolic acidosis: guidelines from a French expert panel.  Ann. Intensive Care   9 , 92 (2019) Jung, B., Martinez, M., Claessens , YE.  et al.  Diagnosis and management of metabolic acidosis: guidelines from a French expert panel.  Ann. Intensive Care   9 , 92 (2019)

11. Steps after Identifying Metabolic Acidosis Check for the degree of respiratory compensation Calculate the anion gaps  WAGMA vs NAGMA Calculate Delta anion gaps for WAGMA Calculate Osmolal Gap for WAGMA Calculate Urinary Anion Gaps for NAGMA

12. Compensatory response of Metabolic Acidosis

13. C heck for the degree of compensation… Respiratory response begins within 30 minutes and is complete by 12 to 24 hours Hasan, A. (2013).  Handbook of Blood Gas/Acid-Base Interpretation.

14. Steps after Identifying Metabolic Acidosis Check for the degree of respiratory compensation Calculate the anion gaps  WAGMA vs NAGMA Calculate Delta anion gaps for WAGMA Calculate Osmolal Gap for WAGMA Calculate Urinary Anion Gaps for NAGMA

15. Calculate Anion Gap Anion gap is calculated by AG = Na + K – (HCO3 + Cl) the normal AG is 10 ± 4 mEq /L (12) The anion gap (AG) is an additional tool in evaluating acid-base disturbances  represents the difference between the serum concentrations of positively charged ions ( cations ) and negatively charged ions ( anions ) Na + K + unmeasured cations = Cl + HCO + unmeasured anions SO… Na + K - Cl – HCO 3 = Unmeasured anions - Unmeasured cations

16. Calculate Anion Gaps

17. Hasan, A. (2013).  Handbook of Blood Gas/Acid-Base Interpretation . Anion gap is widened because the sum of measured cations ([Na+] + [K+]) significantly exceeds the sum of the measured anions ([HCO3 – + [Cl–])  presence of an excess of unmeasured anions in the blood

18. Electrolytes That Influence the Anion Gap Hasan, A. (2013).  Handbook of Blood Gas/Acid-Base Interpretation .

19. Metabolic Acidosis high AG Hasan, A. (2013).  Handbook of Blood Gas/Acid-Base Interpretation .

20. Metabolic Acidosis normal AG

21. Normal Anion Gap Metabolic Acidosis (NAGMA) Hasan, A. (2013).  Handbook of Blood Gas/Acid-Base Interpretation .

22. Don’t forget of hypoalbuminemia… Physiological AG  composed of phosphate and albumin Hypoalbuminemia  decrease in AG Taking the albumin level into account in the calculation of AG unmasks plasma acids when there is hypoalbuminemia AG = Na −(Cl +HCO3 )= 12 ± 4 mmol/L cAG = AG + (4.5−[albumin level]) × 2.5 Jung, B., Martinez, M., Claessens , YE.  et al.  Diagnosis and management of metabolic acidosis: guidelines from a French expert panel.  Ann. Intensive Care   9 , 92 (2019)

23. Steps after Identifying Metabolic Acidosis Check for the degree of respiratory compensation Calculate the anion gaps  WAGMA vs NAGMA Calculate Delta anion/ bicarbonat gaps for WAGMA Calculate Osmolal Gap for WAGMA Calculate Urinary Anion Gaps for NAGMA

24. Bicarbonate gaps/Delta ratio In WAGMA  decrease in the bicarbonate that accounts for the increase in the anion gap. If ↓ bicarbonate is disproportionate to the ↓ anion gap  presence of an additional acid-base disorder . The difference between the increase in the anion gap (ΔAG) and the decrease in the bicarbonate (ΔHCO 3 − ) is termed the bicarbonate gap. increase in anion gap = decrease in the serum bicarbonate (Note that the venous CO2 reflects serum bicarbonate levels). Example: the anion gap has increased by 8 mEq /L, the serum bicarbonate is also expected to fall by 8 mEq /L

25. Steps after Identifying Metabolic Acidosis Check for the degree of respiratory compensation Calculate the anion gaps  WAGMA vs NAGMA Calculate Delta anion gaps for WAGMA Calculate Osmolal Gap for WAGMA Calculate Urinary Anion Gaps for NAGMA

26. Osmolarity and Osmolality Formula for calculation of osmolarity: (2xNa) + glucose/18 + BUN/2.8 Hasan, A. (2013).  Handbook of Blood Gas/Acid-Base Interpretation.

27. Osmolar Gap The extent by which the measured value of solutes ( osmolality ) exceeds the calculated value of solutes ( osmolarity ) is termed the osmolar gap Osmolar gap = measured osmolality – calculated osmolarity In the absence of additional solute  measured Osmolality will approximate the calculated Osmolarity , i.e., 290 mOsm /kg. Hasan, A. (2013).  Handbook of Blood Gas/Acid-Base Interpretation.

28. Conditions causing Osmolar Gap Hasan, A. (2013).  Handbook of Blood Gas/Acid-Base Interpretation.

29. Steps after Identifying Metabolic Acidosis Check for the degree of respiratory compensation Calculate the anion gaps  WAGMA vs NAGMA Calculate Delta anion gaps for WAGMA Calculate Osmolal Gap for WAGMA Calculate Urinary Anion Gaps for NAGMA

30. Urinary Anion gaps UAG helps distinguish between the principal causes of NAGMA Hasan, A. (2013).  Handbook of Blood Gas/Acid-Base Interpretation.

31. Urinary Anion gaps Hasan, A. (2013).  Handbook of Blood Gas/Acid-Base Interpretation.

32. WHY Metabolic Acidosis Matters?? Animal studies : reduced cardiac contractility at pH < 7.1 when lactic acid was administered to dogs Animal studies : hydrochloric acid administered to rats  NO production increased  vasodilation  reduced systemic blood pressure Fatal arrhythmias induced by acidosis reported in an experimental model C linical studies in humans have not yet demonstrated a causal relationship between metabolic acidosis and cardiovascular dysfunction Huang YG,et al. Cardiovascular responses to graded doses of three catecholamines during lactic and hydrochloric acidosis in dogs. Br J Anaesth . 1995;74:583–90. Pedoto A, et al. Acidosis stimulates nitric oxide production and lung damage in rats. Am J Respir Crit Care Med. 1999;159:397–402. Orchard CH, Cingolani HE. Acidosis and arrhythmias in cardiac muscle. Cardiovasc Res. 1994;28:1312–9.

33. WHY Metabolic Acidosis Matters?? Reduced left ventricular contractility Arrhythmias Arterial vasodilation and venoconstriction Impaired responsiveness to catecholamine vasopressors Huang YG,et al. Cardiovascular responses to graded doses of three catecholamines during lactic and hydrochloric acidosis in dogs. Br J Anaesth . 1995;74:583–90. Pedoto A, et al. Acidosis stimulates nitric oxide production and lung damage in rats. Am J Respir Crit Care Med. 1999;159:397–402. Orchard CH, Cingolani HE. Acidosis and arrhythmias in cardiac muscle. Cardiovasc Res. 1994;28:1312–9.

34. Clinical Manifestations of Metabolic Acidosis Metabolic acidosis affects almost all organ systems

35. HOW we manage metabolic acidosis in CVCU ? Basic Principle: TREAT underlying cause ! M aking sure vascular volume and cardiac output are normal, in addition to ensuring adequate oxygenation These actions allow time for the normal metabolism of organic acids (lactic acid and ketoacids), and allow time for the kidneys to generate bicarbonate to replace losses Swenson ER: Metabolic acidosis. Respir Care 46:342–353, 2001

36. Lac tic Acidosis

37. Lactic Acidosis Aim: r eversal of the underlying disease ( eg , shock, sepsis) C ombination of overproduction and underutilization  overwhelm any attempt to increase the serum bicarbonate with exogenous bicarbonat U nless the pathologic process causing the excessive production of lactic acid can be reversed  any beneficial effect of exogenous bicarbonate will be transient

38. Bicarbonat therapy in Lactic Acidosis Role of bicarbonate therapy is controversial Two small randomized, crossover, single center trials Cooper et al.  sodium bicarbonate administration increased pH and PCO2 with no change in blood pressure or cardiac output Mathieu et al.  sodium bicarbonate administration increase in pH but no change in hemodynamic parameters, including cardiac index Cooper DJ, et al .1990. Bicarbonate does not improve hemodynamics in critically III patients who have lactic acidosis: a prospective, controlled clinical study. Ann Intern Med;112:492–8. Mathieu D, Neviere R, et al . 1991. Effects of bicarbonate therapy on hemodynamics and tissue oxygenation in patients with lactic acidosis: a prospective, controlled clinical study. Crit Care Med. 1991;19:1352–6

39. When to give Bicarbonate therapy? When lactic acidosis has generated severe acidemia ( ie , pH less than 7.1 )  hemodynamic instability due to reduced LV contractility, vasodilation, impaired responsiveness to catecholamines In patients with less severe acidemia ( eg , pH 7.1 to 7.2 ) and severe acute kidney injury ( ie , a twofold or greater increase in serum creatinine or oliguria )  bicarbonate therapy can potentially prevent the need for dialysis and may improve survival Kraut JA, Madias NE. Treatment of acute metabolic acidosis: a pathophysiologic approach. Nat Rev Nephrol 2012; 8:589. Jaber S, et al. Sodium bicarbonate therapy for patients with severe metabolic acidaemia in the intensive care unit (BICAR-ICU): a multicentre , open label,randomised controlled, phase 3 trial. Lancet 2018; 392:31.

40. Evans L, et al . Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Crit Care Med. 2021 Nov 1;49(11):e1063-e1143. Jung, B., Martinez, M., Claessens , YE.  et al.  Diagnosis and management of metabolic acidosis: guidelines from a French expert panel.  Ann. Intensive Care   9 , 92 (2019)

41. How to give Bicarbonat therapy weight (kg) x base deficit /3  give half of dose, another half expected to be corrected endogenously HCO3 ( mEq ) required = 0.5 x weight (kg) x [24 - serum HCO3 ( mEq /L)]  give in 2-4 hours Give 1 to 2 mEq /kg sodium bicarbonate as IV bolus  repeat this dose after 30 to 60 minutes if the pH is still less than 7.1 OR OR Wiederkehr, M., Emmett, M. 2023. Bicarbonate therapy in lactic acidosis. Uptodate Reddi, A. S. (2018).  Fluid, Electrolyte and Acid-Base Disorders.  

42. Potential harm of Bicarbonate therapy Increased arterial and tissue capillary partial pressure of carbon dioxide (PCO2) Acceleration of lactate generation Hypernatremia Extracellular fluid (ECF) volume expansion Reddi, A. S. (2018).  Fluid, Electrolyte and Acid-Base Disorders.  doi:10.1007/978-3-319-60167-0 

43. Things to remember ….. Assure that the patient is adequately ventilated  prerequisite to the effective use of exogenous bicarbonate in patients with lactic acidosis S erum electrolytes and blood pH should be measured 30 to 60 minutes later , and the dose of sodium bicarbonate can be repeated if severe lactic acidosis (pH less than 7.1) persists There is “ potential bicarbonate ” concept

44. Renal A cidosis

45. Uremic/Renal Acidosis Acidosis in uremic patients results from a failure by the kidneys to excrete acids H+ elimination is a direct secretory function of the renal tubules. The ability to excrete NH4 + , HSO4 − , and HPO4 −2  varies directly with the glomerular filtration rate (GFR) Any pathologic process affecting the GFR increases HSO4 and HPO4 −2 , resulting in an increased AG

46. The anatomic site of the pathology determines the type of acidosis that develops

47. When to do RRT for AKI+metabolic acidosis?? N o clear consensus of clinical indications for RRT AKIKI trial , IDEAL-ICU trial , and STARRT-AKI trial  metabolic acidosis with severe acidemia  one of the absolute indications AKIKI trial  compared early initiation of RRT in stage 3 AKI and delayed initiation  absolute indications : severe acidemia with pH < 7.15 , either metabolic acidosis or mixed acidosis IDEAL-ICU trial  patients with septic shock and stage 3 AKI. A bsolute indications for RRT : metabolic acidosis with pH < 7.15 and base deficit > 5 mEq /l or HCO3 < 18 mEq /l Gaudry S, et al. Initiation strategies for renal-replacement therapy in the intensive care unit. N Engl J Med. 2016;375:122–33. Barbar SD, et al. Timing of renal-replacement therapy in patients with acute kidney injury and sepsis. N Engl J Med. 2018;379:1431–42. STARRT-AKI Investigators, et al. Timing of initiation of renal-replacement therapy in acute kidney injury. N Engl J Med. 2020;383:240–51.

48. Diabetic Ketoacidosis

49. Is measurement of capillary blood ketones more efective than measurement of urine ketones in diagnosing ketoacidosis? Capillary blood ketones rather than urine ketones should be measured when diagnosing ketoacidosis (GRADE 1+, STRONG AGREEMENT) YES Various cut off  B lood ketones above 3 mmol/L associated with hyperglycemia constitute a good diagnostic criterion of DKA Jung, B., Martinez, M., Claessens , YE.  et al.  Diagnosis and management of metabolic acidosis: guidelines from a French expert panel.  Ann. Intensive Care   9 , 92 (2019)

50. Chua et al (2011)  sodium bicarbonate did not shorten the duration of acidosis, ketosis, or glycemic levels Chua et al (2011)  a lack of rigorous RCT that assessed patient-centered outcomes in DKA Beneficial effects of sodium bicarbonate administration for DKA might be limited Bicarbonat therapy in DKA Chua HR,. Bicarbonate in diabetic ketoacidosis—a systematic review. Ann Intensive Care. 2011;1:23

51. Role of mechanical ventilation in metabolic acidosis P atients are often struggling to lower their PaCO2 to achieve some degree of hyperventilation to compensate for the metabolic acidosis As a consequence, these patients are at risk for developing respiratory muscle fatigue I n this situation, mechanical ventilation is indicated to meet the minimum goal of compensated hypocapnia Non Invasive vs Invasive Ventilation ??  whether the patient meets the criteria for one or another

52. The aim of ventilation is not to normalize pH . A target pH greater than or equal to 7.15 seems reasonable Medical treatment of metabolic acidosis and of its cause should be envisaged concomitantly, as ventilatory compensation can only be symptomatic and temporary Jung, B., Martinez, M., Claessens , YE.  et al.  Diagnosis and management of metabolic acidosis: guidelines from a French expert panel.  Ann. Intensive Care   9 , 92 (2019)

53. Should minute ventilation be increased in mechanically ventilated patients with metabolic acidosis? Experts suggest compensating for acidemia by increasing respiratory frequency without inducing intrinsic PEEP, with a maximum of 35 cycles/min and/or a tidal volume up to 8 mL/ kg of body weight, and by monitoring plateau pressure Jung, B., Martinez, M., Claessens , YE.  et al.  Diagnosis and management of metabolic acidosis: guidelines from a French expert panel.  Ann. Intensive Care   9 , 92 (2019)

54. Initial Ventilatory Setting in VC-CMV

55. Before measuring VT, we need to measure….

56. What to do next? ….. After those initial setting, don’t forget to re-measure BGA 30 minutes later Determine minimal expected pCO2 compensation ( Winter formula ) If pCO2 already fall within expected range  continue previous setting. DON’T forget to address underlying cause of metabolic acidosis If pCO2 level fall higher than expected  increase MV to reduce pCO2 into target  using equation pCO2xMV = pCO2xMV If pCO2 fall lower than expected  decrease MV to increase pCO2 into target  using equation pCO2xMV = pCO2xMV

57. Expected compensation of CO2 in Acute Metabolic Acidosis Winter’s Formula: PCO 2 = 1.5(HCO 3 ) +8  2 Use above formula to determine pCO2 target during MV by putting pCO2 target into next equation Known PaCO2 x Known MV = Desired PaCO2 x Desired MV

58. Equation to remember….. If rate (f) constant and change TV , equation becomes  Desired VT = Known PaCO2 x Known VT Desired / PaCO2 If TV constant and change f , equation becomes  Desired f = Known PaCO2 x Known f Desired / PaCO2 Known PaCO2 x Known MV = Desired PaCO2 x Desired MV

59. Acid-base physiology Blood pH is under constant threat by endogenous acid and base loads If not removed, these loads can cause severe disturbances in blood pH and thus impair cellular function Three important regulatory systems prevent changes in pH and thus maintain blood pH in the normal range These protective systems are buffers, lungs, and kidneys

60. Buffer All acids that are produced must be removed from the body in order to maintain normal blood pH The kidneys eliminate most of these acids, it takes hours to days to complete the process Buffers (both cellular and extracellular) are the first line of defense against wide fluctuations in pH

61. Buffer The main buffers in blood are bicarbonate, haemoglobin , plasma proteins and phosphates Mainly, the buffer involves carbonic acid (H 2 CO 3 ), a weak acid, and bicarbonate ion (HCO 3- ), the conjugate base

62. Bicarbonate Buffer System

63. Other Blood Buffer Systems

64. Lungs The second line of defense against pH disturbance by expelling the CO 2 that is produced by cellular metabolism through the lungs Alveolar ventilation Maintains normal pCO 2 to prevent an acute change in pH Controlled by chemoreceptors located centrally in the medulla and peripherally in the carotid body and aortic arch Blood [H+] and pCO 2 are important regulators The chemoreceptors sense the changes in [H+] or pCO 2 and alter alveolar ventilatory rate

65. Kidneys In a healthy individual, kidneys excrete the acid load and maintain plasma [HCO3−] around 24 mEq /L The maintenance of [HCO 3 − ] is achieved by three renal mechanisms: Reabsorption of filtered HCO 3 − Generation of new HCO 3 − by titratable acid (TA) excretion Formation of HCO 3 − from generation of NH 4 +

66. Case Study 1 Male, 53 y.o , with Dx: CAD 3VD, CHF NYHA II EF 20%, LV thrombus CC : fatigue, dyspnea on effort VS : BP 95/65, BP 102, RR 22, SatO2 98% Lab : Hb 3.7 , Ht 11.6, Eritrosit 1.2, NLR 10.3, Leukosit 17540 , Thrombosit 281, INR 49 , APTT 154, Ur 54, BUN 25.5, Cr 0.81, eGFR 106, GDS 223, Na 134, K 4.9, Cl 101 BGA : pH 7.2 , pCO2 17.9 , PO2 352.2, HCO3 7.1 , BE -18.5 , Saturasi 96, As laktat >20 Rx : Bisoprolol, Lansoprazole, Miniaspi , Simvastatin, Warfarin, Ramipril, Spironolactone, Furosemid