ACID-BASE BALANCE ACID-BASE BALANCE

By:By:

Husnil KadriHusnil Kadri

Biochemistry Departement

Medical Faculty Of Andalas University

Padang

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CARA CARA TRADISIONAL :TRADISIONAL :

Hendersen-Hendersen-HasselbalchHasselbalch(1909) (1909)

3

pH pH = 6.1 + log= 6.1 + log[HCO[HCO33

--]]

pCOpCO22

GINJALGINJAL

PARUPARU

BASA BASA

ASAMASAM CO2

HCO3HCO3

CO2

KompensasiKompensasi

NormalNormal

NormalNormal

4

Carbonic acid/bicarbonate buffer systemCarbonic acid/bicarbonate buffer system

• The pKa 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

H2CO3 H+ + HCO3-

Carbonic acid Bicarbonate ion

pKa = 6.1

ECF:

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• pH = pKa + log [HCO3-]/[H2CO3]

• pH = pKa + log [HCO3-]/0.03 x PCO2

• 7.4 = 6.1 + log 20 / 1

• 7.4 = 6.1 + 1.3

• Plasma pH equals 7.4 when buffer ratio is 20/1

• The solubility constant of CO2 is 0.03

Henderson-Hasselbalch equationHenderson-Hasselbalch equation

DISORDER pH PRIMER RESPON KOMPENSAS

I

ASIDOSIS 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.

DUA VARIABELDUA VARIABEL

pH atau [HpH atau [H++] DALAM PLASMA ] DALAM PLASMA DITENTUKAN OLEHDITENTUKAN OLEH

VARIABELVARIABELINDEPENDENINDEPENDEN

Stewart PA. Can J Physiol Pharmacol 61:1444-1461, 1983.

VARIABELVARIABELDEPENDENDEPENDEN

Cara Stewart ;Cara Stewart ;

Strong IonsStrong IonsDifferenceDifference

pCOpCO22

ProteinProteinConcentrationConcentration

pHpH

INDEPENDENT VARIABLESINDEPENDENT VARIABLES DEPENDENT VARIABLESDEPENDENT VARIABLES

VARIABEL INDEPENDENVARIABEL INDEPENDEN

COCO22 STRONG ION STRONG ION DIFFERENCEDIFFERENCE

WEAK ACIDWEAK ACID

pCOpCO22 SIDSID AAtottot

DEPENDENT VARIABLESDEPENDENT VARIABLES

HH++

OHOH--

CO3CO3-- AA--

AHAH

HCO3-HCO3-

COCO22 Didalam plasma berada Didalam plasma berada

dalam 4 bentukdalam 4 bentuk sCOsCO22 (terlarut) (terlarut)

HH22COCO33 asam karbonat asam karbonat

HCOHCO33-- ion bikarbonat ion bikarbonat

COCO332-2- ion karbonat ion karbonat

Rx dominan dari CORx dominan dari CO22 adalah rx adalah rx

absorpsi OHabsorpsi OH-- hasil disosiasi air hasil disosiasi air dengan melepas Hdengan melepas H++..

Semakin tinggi pCOSemakin tinggi pCO22 semakin semakin

banyak Hbanyak H++ yang terbentuk. yang terbentuk. Ini yg menjadi dasar dari Ini yg menjadi dasar dari

terminologi “respiratory acidosis,” terminologi “respiratory acidosis,” yaitu pelepasan ion hidrogen akibat yaitu pelepasan ion hidrogen akibat pCO pCO22

COCO22

Definisi:Definisi:Strong ion difference adalah ketidakseimbangan Strong ion difference adalah ketidakseimbangan muatanmuatan dari ion-ion kuat. Lebih rinci lagi, SID adalah jumlah dari ion-ion kuat. Lebih rinci lagi, SID adalah jumlah

konsentrasi basa kation kuat dikurangi jumlah dari konsentrasi basa kation kuat dikurangi jumlah dari konsentrasi asam anion kuat. Untuk definisi ini semua konsentrasi asam anion kuat. Untuk definisi ini semua konsentrasi ion-ion diekspresikan dalam ekuivalensi konsentrasi ion-ion diekspresikan dalam ekuivalensi (mEq/L).(mEq/L).

Semua ion kuat akan terdisosiasi sempurna jika berada didalam Semua ion kuat akan terdisosiasi sempurna jika berada didalam larutan, misalnya ion natrium (Nalarutan, misalnya ion natrium (Na++), atau klorida (Cl), atau klorida (Cl--). Karena ). Karena selalu berdisosiasi ini maka ion-ion kuat tersebut tidak selalu berdisosiasi ini maka ion-ion kuat tersebut tidak berpartisipasi dalam reaksi-reaksi kimia. Perannya dalam kimia berpartisipasi dalam reaksi-reaksi kimia. Perannya dalam kimia asam basa hanya pada hubungan elektronetraliti.asam basa hanya pada hubungan elektronetraliti.

Gamblegram

NaNa++

140140

KK+ + 44CaCa++++

MgMg++++

ClCl--

102102

KATION ANION

SIDSID

STRONG ION STRONG ION DIFFERENCEDIFFERENCE

[Na+] + [K+] + [kation divalen] - [Cl-] - [asam organik kuat-]

[Na+] + [K+] - [Cl-] = [SID]

140 mEq/L + 4 mEq/L - 102 mEq/L = 34 mEq/L

SIDSID(–) ((++))

[H[H++]] [OH[OH--]]

Dalam cairan biologis (plasma) dgn suhu 370C, SID hampir selalu positif, biasanya berkisar 30-40 mEq/Liter

AsidosisAsidosis AlkalosisAlkalosis

Konsentrasi [H+]

Kombinasi protein dan posfat disebut asam lemah total (total weak acid) [Atot]. Reaksi disosiasinya adalah:

[A[Atottot] (KA) = [A] (KA) = [A--].[H].[H++]]

[Protein H] [Protein-] + [H+]

WEAK ACIDWEAK ACID

disosiasi

Gamblegram

NaNa++

140140

KK+ + 44CaCa++++

MgMg++++

ClCl--

102102

HCOHCO33--

2424

KATION ANION

SIDSID

Weak acidWeak acid(Alb-,P-)(Alb-,P-)

NaNa140140

KKMgMgCaCa

ClCl102102

PPAlbAlb

HCOHCO33 = 24 = 24

ClCl115115

PPAlbAlb

HCOHCO33--

Asidosis hiperklore

mi

SID nSID

ClCl102102

Laktat/keto=UA

Keto/laktat

asidosisCLCL9595

PPAlbAlb

SID

Alkalosis hipoklore

miKATIONKATION ANIONANION

H3O+ = H+ = 40 mEq/LHCOHCO33

--

HCO3-

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]

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/L102/1/2 = 204 mEq/L SID = 76 mEq/L

1 liter ½ liter

KEKURANGAN AIR - WATER DEFICITKEKURANGAN AIR - WATER DEFICITDiuretic

Diabetes Insipidus

Evaporasi

SID : 38 SID : 38 76 = 76 = alkalosisalkalosis

ALKALOSIS 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 = AcidosisAcidosis

ASIDOSIS DILUSIASIDOSIS DILUSI

Plasma

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

SID = 45 mEq/L 2 liter

ALKALOSIS HIPOKLOREMIKALKALOSIS HIPOKLOREMIK

SID 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 HIPERKLOREMIK

SID 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/L

Cl- = (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 laktat

Laktat 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 diberikan NaCl 0.9%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

Anion Gap

• Described by Gamble in 1939• Electroneutrality

• Na+, Cl-, and HCO3 are measured ions

Na + UC = Cl + HCO3 + UA

UC = Sum of unmeasured cations

UA = Sum of unmeasured anions

Anion Gap

Unmeasured Cations:• total 11 mEq/L

– Potassium 4– Calcium 5– Magnesium 2

Unmeasured Anions:• total 23 mEq/L

– Sulfates 1– Phosphates 2– Albumin 16– Lactic acid 1– Org. acids 3

Anion Gap

Na + UC = Cl + HCO3 + UA 140 + 11 = 104 + 24 + 23

151 = 151

UA – UC = Na - (Cl + HCO3);Anion Gap = Na - (Cl + HCO3)

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 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

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

Increased Anion GapNormal = 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)

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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

• 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

Change in Anion Gap vs HCO3

• In simple AG Metabolic Acidosis – decrease in plasma bicarbonate = increase in

AG

Anion Gap = 1

HCO3

• Helpful in identifying mixed disorders

Respiratory Compensationfor

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• PCO2 seldom > 50-55

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ReferenceReference1. Achmadi, A., George, YWH., Mustafa, I. Pendekatan “Stewart” Pendekatan “Stewart”

Dalam Fisiologi Keseimbangan Asam Basa. 2007Dalam Fisiologi Keseimbangan Asam Basa. 20072. Beaudoin, D. Electrolytes and ion sensitive electrodes. PPT.

2003.3. Ivkovic, A ., Dave, R. Renal review. PPT4. Kersten. Fluid and electrolytes. PPT.5. Marieb, EN. Fluid, electrolyte, and acid-base balance. PPT.

Pearson Education, Inc. 20046. Rashid, FA. Respiratory mechanism in acid-base homeostasis.

PPT. 2005.7. Silverthorn, DU. Integrative Physiology II: Fluid and Electrolyte

Balance. Chapter 20, part B. Pearson Education, Inc. 20048. Smith, SW. Acid-Base Disorders. www.acid-base.com