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ACID-BASE BALANCE By: Husnil Kadri Biochemistry Departement Medical Faculty Of Andalas University Padang.

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Presentasi berjudul: "ACID-BASE BALANCE By: Husnil Kadri Biochemistry Departement Medical Faculty Of Andalas University Padang."— Transcript presentasi:

1 ACID-BASE BALANCE By: Husnil Kadri Biochemistry Departement Medical Faculty Of Andalas University Padang

2 2 CARA TRADISIONAL : Hendersen-Hasselbalch (1909)

3 3 pH = log [HCO 3 - ] pCO 2  pCO 2 GINJAL PARU BASA ASAM CO 2 HCO 3 CO 2 Kompensasi Normal Normal

4 4 Carbonic acid/bicarbonate buffer system The pK a of carbonic acid is 6.1 Carbonic acid is the major buffer in ECF The pH of blood can be determined using the Henderson-Hasselbalch equation H 2 CO 3  H + + HCO 3 - Carbonic acidBicarbonate ion pKa = 6.1 ECF:

5 5 pH = pK a + log [HCO 3 - ]/[H 2 CO 3 ] pH = pK a + log [HCO 3 - ]/0.03 x PCO = log 20 / = Plasma pH equals 7.4 when buffer ratio is 20/1 The solubility constant of CO 2 is 0.03 Henderson-Hasselbalch equation

6 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

7 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.

8 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.

9 DUA VARIABEL pH atau [H + ] DALAM PLASMA DITENTUKAN OLEH VARIABELINDEPENDEN Stewart PA. Can J Physiol Pharmacol 61: , VARIABEL VARIABELDEPENDEN Cara Stewart ;

10 Strong Ions Difference pCO 2 ProteinConcentration  pH INDEPENDENT VARIABLES DEPENDENT VARIABLES

11 VARIABEL INDEPENDEN CO 2 STRONG ION DIFFERENCE WEAK ACID pCO 2 SID A tot

12 DEPENDENT VARIABLES H+H+H+H+ OH - CO3 - A-A-A-A- AH HCO3-

13 CO 2 Didalam plasma berada dalam 4 bentuk sCO 2 (terlarut) sCO 2 (terlarut) H 2 CO 3 asam karbonat H 2 CO 3 asam karbonat HCO 3 - ion bikarbonat HCO 3 - ion bikarbonat CO 3 2- ion karbonat CO 3 2- ion karbonat Rx dominan dari CO 2 adalah rx absorpsi OH - hasil disosiasi air dengan melepas H +. Rx dominan dari CO 2 adalah rx absorpsi OH - hasil disosiasi air dengan melepas H +. Semakin tinggi pCO 2 semakin banyak H + yang terbentuk. Semakin tinggi pCO 2 semakin banyak H + yang terbentuk. Ini yg menjadi dasar dari terminologi “respiratory acidosis,” yaitu pelepasan ion hidrogen akibat  pCO 2 Ini yg menjadi dasar dari terminologi “respiratory acidosis,” yaitu pelepasan ion hidrogen akibat  pCO 2 CO 2

14 STRONG ION DIFFERENCE Definisi: Strong ion difference adalah ketidakseimbangan muatan dari ion-ion kuat. Lebih rinci lagi, SID adalah jumlah konsentrasi basa kation kuat dikurangi jumlah dari konsentrasi asam anion kuat. Untuk definisi ini semua konsentrasi ion-ion diekspresikan dalam ekuivalensi (mEq/L). Semua ion kuat akan terdisosiasi sempurna jika berada didalam larutan, misalnya ion natrium (Na + ), atau klorida (Cl - ). Karena selalu berdisosiasi ini maka ion-ion kuat tersebut tidak berpartisipasi dalam reaksi-reaksi kimia. Perannya dalam kimia asam basa hanya pada hubungan elektronetraliti.

15 Gamblegram Na K + 4 Ca ++ Mg ++ Cl KATIONANION SID STRONG ION DIFFERENCE [Na + ] + [K + ] + [kation divalen] - [Cl - ] - [asam organik kuat - ] [Na+] + [K+] - [Cl-] = [SID] 140 mEq/L + 4 mEq/L mEq/L = 34 mEq/L

16 SKETSA HUBUNGAN ANTARA SID,H + DAN OH - SID (–)(–) (+)(+)(+)(+) [H + ] [OH - ] Dalam cairan biologis (plasma) dgn suhu 37 0 C, SID hampir selalu positif, biasanya berkisar mEq/Liter AsidosisAlkalosis Konsentrasi [H+]

17 Kombinasi protein dan posfat disebut asam lemah total (total weak acid)  [Atot]. Reaksi disosiasinya adalah: [A tot ] (KA) = [A - ].[H + ] [Protein H] [Protein-] + [H+] WEAK ACID disosiasi

18 Gamblegram Na K + 4 Ca ++ Mg ++ Cl HCO KATIONANION SID Weak acid (Alb-,P-)

19 Na140K Mg Ca Cl102 P Alb HCO 3 = 24 Cl115 P Alb HCO 3 -  Asidosis hiperkloremi SID n SID  Cl102 Laktat/keto=UA Keto/laktat asidosis CL  95 P Alb SID  Alkalosis hipokloremi KATIONANION APLIKASI H 3 O + = H + = 40 mEq/L HCO 3 -  HCO 3 - 

20 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):

21 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):

22 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

23 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

24 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

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

26 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

27 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%

28 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

29 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

30 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

31 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

32 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

33 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

34 Anion Gap Described by Gamble in 1939 Electroneutrality Na+, Cl-, and HCO 3 are measured ions Na + UC = Cl + HCO 3 + UA UC = Sum of unmeasured cations UA = Sum of unmeasured anions

35 Anion Gap Unmeasured Cations: total 11 mEq/L –Potassium4 –Calcium5 –Magnesium2 Unmeasured Anions: total 23 mEq/L –Sulfates1 –Phosphates2 –Albumin16 –Lactic acid1 –Org. acids3

36 Anion Gap Na + UC = Cl + HCO 3 + UA = = 151 UA – UC = Na - (Cl + HCO3); Anion Gap = Na - (Cl + HCO3)

37 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.

38 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).

39 Non anion Gap Acidosis: Anion gap = 8-12 mmol/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

40

41 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)

42 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

43 Increased Anion Gap Normal = 8-15 May differ institutionally “ion specific electrodes” Accumulation of organic acids (ketones, lactate) Toxic Ingestions –methanol, ethylene glycol, salicylates Reduced inorganic acid excretion –phosphates, sulfates Decrease in unmeasured cations (unusual)

44 44 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 Other etiologies of low AG: –Low K, Mg, Ca, increased globulins (Mult. Myeloma), I intoxication Negative AG –more unmeasured cations than unmeasured anions –Bromide, Iodide, Multiple Myeloma

45 Change in Anion Gap vs HCO 3 In simple AG Metabolic Acidosis –decrease in plasma bicarbonate = increase in AG Anion Gap = 1 HCO 3 Helpful in identifying mixed disorders

46 Respiratory Compensation for Metabolic Acidosis: Occurs rapidly Hyperventilation –“Kussmaul Respirations” –Deep > rapid (high tidal volume) Is not Respiratory Alkalosis Metabolic Alkalosis: Calculation not as accurate Hypoventilation Not Respiratory Acidosis Restricted by hypoxemia PCO 2 seldom > 50-55

47 47Reference Pendekatan “Stewart” Dalam Fisiologi Keseimbangan Asam Basa Achmadi, A., George, YWH., Mustafa, I. Pendekatan “Stewart” Dalam Fisiologi Keseimbangan Asam Basa Beaudoin, D. Electrolytes and ion sensitive electrodes. PPT Ivkovic, A., Dave, R. Renal review. PPT 4.Kersten. Fluid and electrolytes. PPT. 5.Marieb, EN. Fluid, electrolyte, and acid-base balance. PPT. Pearson Education, Inc Rashid, FA. Respiratory mechanism in acid-base homeostasis. PPT Silverthorn, DU. Integrative Physiology II: Fluid and Electrolyte Balance. Chapter 20, part B. Pearson Education, Inc Smith, SW. Acid-Base Disorders.


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