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

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Presentation on theme: "ACID-BASE DISORDERS dr. Husnil Kadri, M.Kes Biochemistry Departement Medical Faculty Of Andalas University Padang."— Presentation transcript:

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

2 Normal values for arterial blood gases Blood Gas ParameterParameter Reported and Symbol Used Normal Value Carbon dioxide tension* PCO 2 35 – 45 mm Hg (average, 40) Oxygen tension*PO 2 80 – 100 mm Hg Oxygen percent saturation SO 2 97 Hydrogen ion concentration* pH7.35 – 7.45 BicarbonateHCO – 26 mmol/L Arterial Blood Gases (ABG) * Indicates measured parameter Normal values may differ slightly in exams

3 DISORDERpHPRIMERRESPON KOMPENSASI ASIDOSIS METABOLIK   HCO 3 -   pCO 2  ALKALOSIS METABOLIK   HCO 3 -   pCO 2  ASIDOSIS RESPIRATORI   pCO 2   HCO 3 -  ALKALOSIS RESPIRATORI   pCO 2   HCO 3 -  GANGGUAN KESEIMBANGAN ASAM-BASA TRADISIONAL

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 ASIDOSISALKALOSIS I. Respiratori  PCO 2  PCO 2 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 RESPIRASI M E T A B O L I K AbnormalpCO2AbnormalSIDAbnormal Weak acid AlbPO4- Alkalosis Asidosis Turun Meningkat Turun kelebihan kekurangan Positifmeningkat Fencl V, Am J Respir Crit Care Med 2000 Dec;162(6): AIR  Anion kuat Cl-UA- Hipo Hiper

9 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 liter½ liter KEKURANGAN AIR - WATER DEFICIT Diuretic Diabetes Insipidus Evaporasi SID : 38  76 = alkalosis ALKALOSIS KONTRAKSI Plasma

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

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

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

13 Na + = 140 mEq/L Cl - = 102 mEq/L SID = 38 mEq/L Na + = 154 mEq/L Cl - = 154 mEq/L SID = 0 mEq/L 1 liter PLASMA + NaCl 0.9% SID : 38  PlasmaNaCl 0.9%

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

15 Na + = 140 mEq/L Cl - = 102 mEq/L SID= 38 mEq/L Cation + = 137 mEq/L Cl - = 109 mEq/L Laktat - = 28 mEq/L SID = 0 mEq/L 1 liter PLASMA + Larutan RINGER LACTATE SID : 38 PlasmaRinger laktat Laktat cepat dimetabolisme

16 2 liter = Normal pH setelah pemberian RINGER LACTATE SID : 34  lebih alkalosis dibanding jika diberikan NaCl 0.9% Na + = ( )/2 mEq/L= 139 mEq/L Cl - = ( )/2 mEq/L = 105 mEq/L Laktat - (termetabolisme) = 0 mEq/L SID = 34 mEq/L Plasma

17 Na + = 140 mEq/L Cl - = 130 mEq/L SID =10 mEq/L Na + = 165 mEq/L Cl - = 130 mEq/L SID = 35 mEq/L 1 liter liter 25 mEq NaHCO3 SID  : 10  35 :  Alkalosis, pH kembali normal  namun mekanismenya bukan karena pemberian HCO 3 - melainkan karena pemberian Na + tanpa anion kuat yg tidak dimetabolisme seperti Cl - sehingga SID   alkalosis Plasma; asidosis hiperkloremik MEKANISME PEMBERIAN NA- BIKARBONAT PADA ASIDOSIS Plasma + NaHCO 3 HCO 3 cepat dimetabolisme

18 Na + K HCO 3 - Cl - HCO 3 - SID NormalKetosis UA = Unmeasured Anion: Laktat, acetoacetate, salisilat, metanol dll. A- A- Keto - SID  K Lactic/Keto asidosis

19 Na NaNa KK K HCO 3 ClClCl SID NormalAcidosisAlkalosis GANGGUAN PD ASAM LEMAH: Hipo/Hiperalbumin - atau P - Alb/P  Alb - /P -  SID  SID  Alkalosis hipoalbumin /hipoposfate mi Asidosis hiperprotein/ hiperposfatemi

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)

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

27 Decreased or Negative Anion Gap Clin J Am Soc Nephrol 2: , 2007 Low protein most important Albumin has many unmeasured negative charges “Normal” anion gap (12) in cachectic person –Indicates anion gap metabolic acidosis 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 28Sources Pendekatan “Stewart” Dalam Fisiologi Keseimbangan Asam Basa. ppt Achmadi, A., George, YWH., Mustafa, I. Pendekatan “Stewart” Dalam Fisiologi Keseimbangan Asam Basa. ppt Magdy. A. Blood Gases and Acid-Base Disorders. ppt 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. base.comwww.acid- base.com


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