ACID-BASE ACID-BASE DISORDERSDISORDERS

dr. Husnil Kadri, M.Kesdr. Husnil Kadri, M.Kes

Biochemistry Departement Biochemistry Departement Medical Faculty Of Andalas Medical Faculty Of Andalas

University University PadangPadang

Normal values for arterial blood gases

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

Arterial Blood Gases (ABG)

* Indicates measured parameter Normal values may differ slightly in exams

DISORDER pH PRIMER RESPON KOMPENSAS

IASIDOSIS ASIDOSIS

METABOLIKMETABOLIK HCO3- pCO2

ALKALOSIS ALKALOSIS METABOLIKMETABOLIK

HCO3- pCO2

ASIDOSIS ASIDOSIS RESPIRATORRESPIRATOR

II

pCO2 HCO3-

ALKALOSIS ALKALOSIS RESPIRATORRESPIRATOR

II

pCO2 HCO3-

GANGGUAN KESEIMBANGAN ASAM-GANGGUAN KESEIMBANGAN ASAM-BASA TRADISIONALBASA TRADISIONAL

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 KLASIFIKASI GANGGUAN KESEIMBANGAN ASAM BASA KESEIMBANGAN ASAM BASA

BERDASARKAN PRINSIP BERDASARKAN PRINSIP STEWARTSTEWART

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 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):2246-51

RESPIRASIRESPIRASI M E T A B O L I KM E T A B O L I K

Abnormal Abnormal pCO2pCO2

AbnormalAbnormalSIDSID

AbnormalAbnormalWeak acidWeak acid

AlbAlb PO4-PO4-

AlkalosisAlkalosis

AsidosisAsidosis

TurunTurun

MeningkatMeningkat

TurunTurun

kelebihankelebihan

kekurangankekurangan

PositifPositif meningkatmeningkat

Fencl V, Am J Respir Crit Care Med 2000 Dec;162(6):2246-51

AIRAIR Anion kuatAnion kuat

Cl-Cl- UA-UA-

HipoHipo

HiperHiper

Na+ = 140 mEq/LCl- = 102 mEq/LSID = 38 mEq/L 140/1/2 = 280 mEq/L

102/1/2 = 204 mEq/L SID = 76 mEq/L1 liter ½ liter

KEKURANGAN AIR - WATER DEFICITKEKURANGAN AIR - WATER DEFICITDiuretic

Diabetes InsipidusEvaporasi

SID : 38 SID : 38 76 = 76 = alkalosisalkalosisALKALOSIS KONTRAKSIALKALOSIS KONTRAKSI

Plasma Plasma

Na+ = 140 mEq/LCl- = 102 mEq/L SID = 38 mEq/L

140/2 = 70 mEq/L102/2 = 51 mEq/L SID = 19 mEq/L

1 liter 2 liter

KELEBIHAN AIR - WATER EXCESSKELEBIHAN AIR - WATER EXCESS

1 Liter H2O

SID : 38 SID : 38 19 = 19 = AcidosisAcidosisASIDOSIS DILUSIASIDOSIS DILUSI

Plasma

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

SID = 45 mEq/L 2 liter

ALKALOSIS HIPOKLOREMIKALKALOSIS HIPOKLOREMIKSID ALKALOSIS

GANGGUAN PD SID:GANGGUAN PD SID:Pengurangan ClPengurangan Cl--

Plasma

Na+ = 140 mEq/L Cl- = 120 mEq/LSID = 20 mEq/L 2 liter

ASIDOSIS HIPERKLOREMIKASIDOSIS HIPERKLOREMIKSID ASIDOSIS

GANGGUAN PD SID:GANGGUAN PD SID:Penambahan/akumulasi Penambahan/akumulasi

ClCl--

Plasma

Na+ = 140 mEq/LCl- = 102 mEq/LSID = 38 mEq/L

Na+ = 154 mEq/LCl- = 154 mEq/LSID = 0 mEq/L1 liter 1 liter

PLASMA + NaCl 0.9%PLASMA + NaCl 0.9%

SID : 38

Plasma NaCl 0.9%

2 liter

ASIDOSIS HIPERKLOREMIK AKIBAT ASIDOSIS HIPERKLOREMIK AKIBAT PEMBERIAN LARUTAN Na Cl 0.9% PEMBERIAN LARUTAN Na Cl 0.9%

=

SID : 19 SID : 19 AsidosisAsidosis

Na+ = (140+154)/2 mEq/L= 147 mEq/LCl- = (102+ 154)/2 mEq/L= 128 mEq/L

SID = 19 mEq/L

Plasma

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

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

1 liter 1 liter

PLASMA + Larutan RINGER PLASMA + Larutan RINGER LACTATELACTATE

SID : 38 SID : 38

Plasma Ringer laktatLaktat cepat

dimetabolisme

2 liter

=

Normal pH setelah pemberian Normal pH setelah pemberian RINGER LACTATE RINGER LACTATE

SID : 34 SID : 34 lebih alkalosis dibanding jika lebih alkalosis dibanding jika diberikan NaCl 0.9% diberikan NaCl 0.9%

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

Plasma

Na+ = 140 mEq/LCl- = 130 mEq/LSID =10 mEq/L

Na+ = 165 mEq/LCl- = 130 mEq/LSID = 35 mEq/L1 liter 1.025

liter

25 mEq NaHCO3

SID SID : 10 : 10 35 : 35 : Alkalosis, pH kembali normal Alkalosis, pH kembali normal namun namun mekanismenya bukan karena pemberian HCOmekanismenya bukan karena pemberian HCO33

-- melainkan karena melainkan karena pemberian Napemberian Na++ tanpa anion kuat yg tidak dimetabolisme seperti Cl tanpa anion kuat yg tidak dimetabolisme seperti Cl--

sehingga SID sehingga SID alkalosis alkalosis

Plasma; asidosis

hiperkloremik

MEKANISME PEMBERIAN NA-BIKARBONAT PADA ASIDOSIS

Plasma + NaHCO3

HCO3 cepat dimetabolis

me

NaNa++ NaNa++

KK

HCO3-

ClCl-- ClCl--

HCO3-

SID

Normal Ketosis

UA = Unmeasured Anion:UA = Unmeasured Anion:Laktat, acetoacetate, salisilat, Laktat, acetoacetate, salisilat,

metanol dll.metanol dll.

A-A-AA--

Keto-

SID KK

Lactic/Keto asidosis

NaNa NaNa NaNa

K K KHCO3

ClCl ClCl ClCl

HCO3HCO3SID

Normal Acidosis Alkalosis

GANGGUAN PD ASAM LEMAH:GANGGUAN PD ASAM LEMAH:Hipo/HiperalbuminHipo/Hiperalbumin-- atau P atau P--

Alb/P Alb/P

AlbAlb--/P/P--

AlbAlb--/P/P--

SIDSID

Alkalosis Alkalosis hipoalbuminhipoalbumin/hipoposfate/hipoposfate

mimi

Asidosis Asidosis hiperprotein/ hiperprotein/

hiperposfatemihiperposfatemi

• 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 = 8-15

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 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

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Pendekatan “Stewart” Dalam Fisiologi Pendekatan “Stewart” Dalam Fisiologi Keseimbangan Asam Basa. ppt. 2007Keseimbangan Asam Basa. ppt. 2007

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3. Paphitou, N. Interpretation of Arterial Blood Gases and Acid-Base Disorders. PPT. 2011.

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5. Smith, SW. Acid-Base Disorders. www.acid-base.com