acid base disorders
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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
28
SourcesSources1. Achmadi, A., George, YWH., Mustafa, I.
Pendekatan “Stewart” Dalam Fisiologi Pendekatan “Stewart” Dalam Fisiologi Keseimbangan Asam Basa. ppt. 2007Keseimbangan 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 acid-base homeostasis. PPT. 2005.
5. Smith, SW. Acid-Base Disorders. www.acid-base.com
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