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Biochemistry Departement Medical Faculty Of Andalas University

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1 Biochemistry Departement Medical Faculty Of Andalas University
ACID-BASE DISORDERS dr. Husnil Kadri, M.Kes Biochemistry Departement Medical Faculty Of Andalas University Padang

2 Normal values for arterial blood gases
Arterial Blood Gases (ABG) Blood Gas Parameter Parameter Reported and Symbol Used Normal Value Carbon dioxide tension* PCO2 35 – 45 mm Hg (average, 40) Oxygen tension* PO2 80 – 100 mm Hg Oxygen percent saturation SO2 97 Hydrogen ion concentration* pH 7.35 – 7.45 Bicarbonate HCO3- 22 – 26 mmol/L * Indicates measured parameter Normal values may differ slightly in exams

3 GANGGUAN KESEIMBANGAN ASAM-BASA TRADISIONAL
DISORDER pH PRIMER RESPON KOMPENSASI ASIDOSIS METABOLIK HCO3-  pCO2  ALKALOSIS METABOLIK HCO3-  pCO2  ASIDOSIS RESPIRATORI pCO2  ALKALOSIS RESPIRATORI pCO2  HCO3- 

4 Normal Compensatory Response
Any primary disturbance in acid-base homeostasis invokes a normal compensatory response. A primary metabolic disorder leads to respiratory compensation, and a primary respiratory disorder leads to an acute metabolic response due to the buffering capacity of body fluids. A more chronic compensation (1-2 days) due to alterations in renal function.

5 Mixed Acid - Base Disorder
Most acid-base disorders result from a single primary disturbance with the normal physiologic compensatory response and are called simple acid-base disorders. In certain cases, however, particularly in seriously ill patients, two or more different primary disorders may occur simultaneously, resulting in a mixed acid-base disorder. The net effect of mixed disorders may be additive (eg, metabolic acidosis and respiratory acidosis) and result in extreme alteration of pH; or they may be opposite (eg, metabolic acidosis and respiratory alkalosis) and nullify each other’s effects on the pH.

6 KLASIFIKASI GANGGUAN KESEIMBANGAN ASAM BASA BERDASARKAN PRINSIP STEWART
Fencl V, Jabor A, Kazda A, Figge J. Diagnosis of metabolic acid-base disturbances in critically ill patients. Am J Respir Crit Care Med 2000 Dec;162(6):

7 KLASIFIKASI ASIDOSIS ALKALOSIS I. Respiratori  PCO2  PCO2
ASIDOSIS ALKALOSIS I. Respiratori  PCO2  PCO2 II. Nonrespiratori (metabolik) 1. Gangguan pd SID a. Kelebihan / kekurangan air  [Na+],  SID  [Na+],  SID b. Ketidakseimbangan anion kuat: i. Kelebihan / kekurangan Cl-  [Cl-],  SID  [Cl-],  SID ii. Ada anion tak terukur  [UA-],  SID 2. Gangguan pd asam lemah i. Kadar albumin  [Alb]  [Alb] ii. Kadar posphate  [Pi]  [Pi] Fencl V, Jabor A, Kazda A, Figge J. Diagnosis of metabolic acid-base disturbances in critically ill patients. Am J Respir Crit Care Med 2000 Dec;162(6):

8 Fencl V, Am J Respir Crit Care Med 2000 Dec;162(6):2246-51
RESPIRASI M E T A B O L I K Abnormal pCO2 Abnormal SID Abnormal Weak acid Alb PO4- AIR  Anion kuat Cl- UA- Turun Alkalosis Turun kekurangan Hipo Asidosis Meningkat kelebihan Hiper Positif meningkat Fencl V, Am J Respir Crit Care Med 2000 Dec;162(6):

9 KEKURANGAN AIR - WATER DEFICIT
Diuretic Diabetes Insipidus Evaporasi Plasma Plasma Na+ = 140 mEq/L Cl- = 102 mEq/L SID = 38 mEq/L 140/1/2 = 280 mEq/L 102/1/2 = 204 mEq/L SID = 76 mEq/L 1 liter ½ liter SID : 38  76 = alkalosis ALKALOSIS KONTRAKSI

10 KELEBIHAN AIR - WATER EXCESS
Plasma 140/2 = 70 mEq/L 102/2 = 51 mEq/L SID = 19 mEq/L Na+ = 140 mEq/L Cl = 102 mEq/L SID = 38 mEq/L 1 Liter H2O 1 liter 2 liter SID : 38  19 = Acidosis ASIDOSIS DILUSI

11 GANGGUAN PD SID: Pengurangan Cl- ALKALOSIS HIPOKLOREMIK
Plasma Na+ = 140 mEq/L Cl- = 95 mEq/L SID = 45 mEq/L 2 liter SID  ALKALOSIS ALKALOSIS HIPOKLOREMIK

12 GANGGUAN PD SID: Penambahan/akumulasi Cl- ASIDOSIS HIPERKLOREMIK
Plasma Na+ = 140 mEq/L Cl- = 120 mEq/L SID = 20 mEq/L 2 liter SID  ASIDOSIS ASIDOSIS HIPERKLOREMIK

13 PLASMA + NaCl 0.9% SID : 38  Plasma NaCl 0.9% 1 liter 1 liter
Na+ = 140 mEq/L Cl- = 102 mEq/L SID = 38 mEq/L Na+ = 154 mEq/L Cl- = 154 mEq/L SID = mEq/L 1 liter 1 liter SID : 38 

14 ASIDOSIS HIPERKLOREMIK AKIBAT PEMBERIAN LARUTAN Na Cl 0.9%
Plasma = Na+ = ( )/2 mEq/L= 147 mEq/L Cl- = ( )/2 mEq/L= 128 mEq/L 2 liter SID = 19 mEq/L SID : 19  Asidosis

15 PLASMA + Larutan RINGER LACTATE Laktat cepat dimetabolisme
Ringer laktat Laktat cepat dimetabolisme Na+ = 140 mEq/L Cl- = 102 mEq/L SID= mEq/L Cation+ = 137 mEq/L Cl- = 109 mEq/L Laktat- = 28 mEq/L SID = mEq/L 1 liter 1 liter SID : 38

16 Normal pH setelah pemberian RINGER LACTATE
Plasma = Na+ = ( )/2 mEq/L= 139 mEq/L Cl- = ( )/2 mEq/L = 105 mEq/L Laktat- (termetabolisme) = mEq/L 2 liter SID = 34 mEq/L SID : 34  lebih alkalosis dibanding jika diberikan NaCl 0.9%

17 MEKANISME PEMBERIAN NA-BIKARBONAT PADA ASIDOSIS
Plasma; asidosis hiperkloremik Plasma + NaHCO3 Na+ = 140 mEq/L Cl- = 130 mEq/L SID =10 mEq/L Na+ = 165 mEq/L Cl- = 130 mEq/L SID = 35 mEq/L 25 mEq NaHCO3 HCO3 cepat dimetabolisme 1 liter 1.025 liter SID  : 10  35 :  Alkalosis, pH kembali normal  namun mekanismenya bukan karena pemberian HCO3- melainkan karena pemberian Na+ tanpa anion kuat yg tidak dimetabolisme seperti Cl- sehingga SID   alkalosis

18 Laktat, acetoacetate, salisilat, metanol dll.
UA = Unmeasured Anion: Laktat, acetoacetate, salisilat, metanol dll. Na+ K HCO3- Na+ K HCO3- SID  SID Keto- A- A- Cl- Cl- Lactic/Keto asidosis Normal Ketosis

19 GANGGUAN PD ASAM LEMAH: Hipo/Hiperalbumin- atau P-
HCO3 Na HCO3 Na HCO3 K K K SID SID SID Alb-/P- Alb-/P- Alb/P  Cl Cl Cl Asidosis hiperprotein/ hiperposfatemi Alkalosis hipoalbumin/hipoposfatemi Normal Acidosis Alkalosis

20 Calculate the anion gap.
Anion gap = Na+ - (Cl- + HCO3 -). Normal anion gap is 8-15 mEq/L.

21 If the anion gap is elevated
Then compare the changes from normal between the anion gap and [HCO3 -]. If the change in the anion gap is greater than the change in the [HCO3 -] from normal, then a metabolic alkalosis is present in addition to a gap metabolic acidosis. If the change in the anion gap is less than the change in the [HCO3 -] from normal, then a non gap metabolic acidosis is present in addition to a gap metabolic acidosis.

22 Anion Gap Acidosis: Anion gap >12 mEq/L; caused by a decrease in [HCO3 -] balanced by an increase in an unmeasured acid ion from either endogenous production or exogenous ingestion (normochloremic acidosis).

23 Non anion Gap Acidosis:
Anion gap = 8-12 mEq/L; caused by a decrease in [HCO3 -] balanced by an increase in chloride (hyperchloremic acidosis). Renal tubular acidosis is a type of non gap acidosis The anion gap is helpful in identifying metabolic gap acidosis, non gap acidosis, mixed metabolic gap and non gap acidosis. If an elevated anion gap is present, a closer look at the anion gap and the bicarbonate helps differentiate among (a) a pure metabolic gap acidosis (b) a metabolic non gap acidosis (c) mixed metabolic gap and non gap acidosis, and (d) a metabolic gap acidosis and metabolic alkalosis.

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25 Increased Anion Gap Normal = 8-15 May differ institutionally
Accumulation of organic acids (ketones, lactate) Toxic Ingestions methanol, ethylene glycol, salicylates Reduced inorganic acid excretion phosphates, sulfates Decrease in unmeasured cations (unusual) Lactate, Keto acids most common organic acids. AG> 35: M, EG, HHC, LA Toxic ingestions: Cyanide, ASA, M, EG, Par, Toluene Reduced Inorganic: Renal failure

26 Increased AG Metabolic Acidosis:
Lactic Acidosis Has many etiologies Cyanide, CO, Toluene, HS Poor perfusion Ethylene glycol Salicylates Methyl salicylate (Oil of wintergreen) Mg salicylate Methanol Uremia/Renal Failure INH, Iron--lactate Paraldehyde Levraut J et al. Int Care Med 23:417, 1997

27 Decreased or Negative Anion Gap Clin J Am Soc Nephrol 2: 162-174, 2007
Low protein most important Albumin has many unmeasured negative charges “Normal” anion gap (12) in cachectic person Indicates anion gap metabolic acidosis 2-2.5 mEq/liter drop in AG for every 1 g drop in albumin Other etiologies of low AG: Low K, Mg, Ca, increased globulins (Mult. Myeloma), Li, Br (bromism), I intoxication Negative AG more unmeasured cations than unmeasured anions Bromide, Iodide, Multiple Myeloma

28 Sources Achmadi, A., George, YWH., Mustafa, I. Pendekatan “Stewart” Dalam Fisiologi Keseimbangan Asam Basa. ppt. 2007 Magdy. A. Blood Gases and Acid-Base Disorders. ppt. 2011 Paphitou, N. Interpretation of Arterial Blood Gases and Acid-Base Disorders. PPT Rashid, FA. Respiratory mechanism in acid-base homeostasis. PPT Smith, SW. Acid-Base Disorders. 28


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