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)

Blood Gas Parameter

Parameter Reported and Symbol Used

Normal Value

Carbon dioxide tension* Oxygen tension* Oxygen percent saturation Hydrogen ion concentration* Bicarbonate
* Indicates measured parameter

PCO2 PO2 SO2 pH HCO3-

35 45 mm Hg (average, 40) 80 100 mm Hg 97 7.35 7.45 22 26 mmol/L

Normal values may differ slightly in exams

GANGGUAN KESEIMBANGAN ASAM-BASA TRADISIONAL

DISORDER ASIDOSIS METABOLIK ALKALOSIS METABOLIK ASIDOSIS RESPIRATORI ALKALOSIS RESPIRATORI pH PRIMER HCO3- HCO3- pCO2 pCO2 RESPON KOMPENSASI pCO2 pCO2 HCO3- HCO3-

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 others 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

KLASIFIKASI
ASIDOSIS I. Respiratori PCO2 ALKALOSIS PCO2

II. Nonrespiratori (metabolik)

1. Gangguan pd SID

a. Kelebihan / kekurangan air

b. Ketidakseimbangan anion kuat: i. Kelebihan / kekurangan Clii. Ada anion tak terukur

[Na+], SID

[Na+], SID

[Cl-], SID [UA-], SID

[Cl-], SID

2. Gangguan pd asam lemah

i. Kadar albumin ii. Kadar posphate [Alb] [Pi] [Alb] [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):2246-51

RESPIRASI
Abnormal pCO2

METABOLIK
Abnormal SID Abnormal Weak acid

AIR

Anion kuat

Alb

PO4-

Cl-

UA-

Alkalosis Asidosis

Turun Meningkat

kekurangan kelebihan

Hipo Hiper Positif

Turun 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

1 liter

140/1/2 = 280 mEq/L 102/1/2 = 204 mEq/L SID = 76 mEq/L

liter

SID : 38 76 = alkalosis ALKALOSIS KONTRAKSI

KELEBIHAN AIR - WATER EXCESS

Plasma
1 Liter H2O
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

2 liter

SID : 38 19 = Acidosis ASIDOSIS DILUSI

GANGGUAN PD SID: Pengurangan ClPlasma

Na+ = 140 mEq/L Cl- = 95 mEq/L SID = 45 mEq/L

2 liter

SID

ALKALOSIS

ALKALOSIS HIPOKLOREMIK

GANGGUAN PD SID: Penambahan/akumulasi ClPlasma

Na+ = 140 mEq/L Cl- = 120 mEq/L SID = 20 mEq/L

2 liter

SID

ASIDOSIS

ASIDOSIS HIPERKLOREMIK

PLASMA + NaCl 0.9%

Plasma
Na+ = 140 mEq/L Cl- = 102 mEq/L SID = 38 mEq/L

NaCl 0.9%
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 SID = 19 mEq/L

2 liter

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

1 liter

Cation+ = 137 mEq/L Cl- = 109 mEq/L Laktat- = 28 mEq/L SID = 0 mEq/L

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 SID = 34 mEq/L

2 liter

SID : 34 lebih alkalosis dibanding jika diberikan NaCl 0.9%

MEKANISME PEMBERIAN NABIKARBONAT PADA ASIDOSIS

Plasma;
asidosis hiperkloremik
25 mEq NaHCO3

Plasma + NaHCO3

Na+ = 140 mEq/L Cl- = 130 mEq/L SID =10 mEq/L

Na+

HCO3 cepat = 165 mEq/L dimetabolisme

1 liter

1.025 liter

Cl- = 130 mEq/L SID = 35 mEq/L

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.

K

HCO3-

SID

HCO3-

SID

KetoA-

A-

Na+ Cl-

Na+ ClLactic/Keto asidosis

Normal

Ketosis

GANGGUAN PD ASAM LEMAH: Hipo/Hiperalbumin- atau PK K K

HCO3 SID

HCO3

SID

HCO3
Alb-/P

SID

Alb-/P-

Alb/P

Na

Na

Cl

Na Asidosis hiperprotein/ hiperposfatemi Cl

Alkalosis hipoalbumin Cl /hipoposfate mi

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 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)

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

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

Sources
1. Achmadi, A., George, YWH., Mustafa, I. Pendekatan Stewart Dalam Fisiologi Keseimbangan Asam Basa. ppt. 2007 2. Magdy. A. Blood Gases and Acid-Base Disorders. ppt. 2011 3. Paphitou, N. Interpretation of Arterial Blood Gases and Acid-Base Disorders. PPT. 2011. 4. Rashid, FA. Respiratory mechanism in acidbase homeostasis. PPT. 2005. 5. Smith, SW. Acid-Base Disorders. www.acidbase.com
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