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Learn about arterial blood gases' normal values, compensation responses, traditional classifications, and Stewart's principle-based categorizations of acid-base imbalances. Explore respiratory and metabolic aspects, anion gap calculations, and common disorders with expert insights.
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ACID-BASE DISORDERS dr. Husnil Kadri, M.Kes Biochemistry Departement Medical Faculty Of Andalas University Padang
Normal values for arterial blood gases Arterial Blood Gases (ABG) Normal values may differ slightly in exams * Indicates measured parameter
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.
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.
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):2246-51
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] KLASIFIKASI 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):2246-51
RESPIRASI M E T A B O L I K Abnormal pCO2 Abnormal SID Abnormal Weak acid Alb PO4- Anion kuat AIR 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):2246-51
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
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
GANGGUAN PD SID:Pengurangan Cl- Plasma Na+ = 140 mEq/L Cl- = 95 mEq/L SID = 45 mEq/L 2 liter SID ALKALOSIS ALKALOSIS HIPOKLOREMIK
GANGGUAN PD SID:Penambahan/akumulasi Cl- Plasma Na+ = 140 mEq/L Cl- = 120 mEq/L SID = 20 mEq/L 2 liter SID ASIDOSIS ASIDOSIS HIPERKLOREMIK
PLASMA + NaCl 0.9% Plasma NaCl 0.9% 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 1 liter SID : 38
ASIDOSIS HIPERKLOREMIK AKIBAT PEMBERIAN LARUTAN Na Cl 0.9% Plasma = Na+ = (140+154)/2 mEq/L= 147 mEq/L Cl- = (102+ 154)/2 mEq/L= 128 mEq/L 2 liter SID = 19 mEq/L SID : 19 Asidosis
PLASMA + Larutan RINGER LACTATE Plasma Ringer laktat Laktat cepat dimetabolisme 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 1 liter SID : 38
Normal pH setelah pemberian RINGER LACTATE Plasma = Na+ = (140+137)/2 mEq/L= 139 mEq/L Cl- = (102+ 109)/2 mEq/L = 105 mEq/L Laktat- (termetabolisme) = 0 mEq/L 2 liter SID = 34 mEq/L SID : 34 lebih alkalosis dibanding jika diberikan NaCl 0.9%
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
UA = Unmeasured Anion: Laktat, acetoacetate, salisilat, metanol dll. Na+ HCO3- HCO3- SID Na+ K K SID Keto- A- A- Cl- Cl- Lactic/Keto asidosis Normal Ketosis
GANGGUAN PD ASAM LEMAH: Hipo/Hiperalbumin- atau P- Na HCO3 Na HCO3 HCO3 Na K K K SID SID SID Alb-/P- Alb-/P- Alb/P Cl Cl Cl Asidosis hiperprotein/ hiperposfatemi Alkalosis hipoalbumin/hipoposfatemi Normal Acidosis Alkalosis
Calculate the anion gap. • Anion gap = Na+ - (Cl- + HCO3 -). • Normal anion gap is 8-15 mEq/L.
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.
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).
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.
Increased Anion GapNormal = 8-15May 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)
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 Increased AG Metabolic Acidosis: Levraut J et al. Int Care Med 23:417, 1997
Decreased or Negative Anion GapClin 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
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. 2011. Rashid, FA. Respiratory mechanism in acid-base homeostasis. PPT. 2005. Smith, SW. Acid-Base Disorders. www.acid-base.com 28