Transcript BASIC APPROACH TO BODY pH - C A R D I O | Community of

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
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
Carbon dioxide
tension*
Bicarbonate
* Indicates measured parameter
HCO3-
22 – 26 mmol/L
Normal values may differ slightly in exams
GANGGUAN KESEIMBANGAN ASAM-BASA
TRADISIONAL
DISORDER
pH
PRIMER
RESPON
KOMPENSASI
ASIDOSIS
METABOLIK

HCO3- 
pCO2 
ALKALOSIS
METABOLIK

HCO3- 
pCO2 
ASIDOSIS
RESPIRATORI

pCO2 
HCO3- 
ALKALOSIS
RESPIRATORI

pCO2 
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 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
KLASIFIKASI
ASIDOSIS
ALKALOSIS
 PCO2
 PCO2
 [Na+],  SID
 [Na+],  SID
i. Kelebihan / kekurangan Cl-
 [Cl-],  SID
 [Cl-],  SID
ii. Ada anion tak terukur
 [UA-],  SID
I. Respiratori
II. Nonrespiratori (metabolik)
1. Gangguan pd SID
a. Kelebihan / kekurangan air
b. Ketidakseimbangan anion
kuat:
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
RESPIRASI
METABOLIK
Abnormal
pCO2
Abnormal
SID
AIR
 Anion kuat
Cl-
Alkalosis
Turun
kekurangan
Hipo
Asidosis
Meningkat
kelebihan
Hiper
Fencl V, Am J Respir Crit Care Med 2000 Dec;162(6):2246-51
Abnormal
Weak acid
Alb
PO4-
UA-
Turun
Positif
meningkat
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
SID : 38  76 = alkalosis
ALKALOSIS KONTRAKSI
½ liter
KELEBIHAN AIR - WATER EXCESS
Plasma
Na+ = 140 mEq/L
Cl- = 102 mEq/L
SID = 38 mEq/L
1 Liter
H2O
1 liter
140/2 = 70 mEq/L
102/2 = 51 mEq/L
SID = 19 mEq/L
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
SID
2 liter
 ALKALOSIS
ALKALOSIS HIPOKLOREMIK
GANGGUAN PD SID:
Penambahan/akumulasi ClPlasma
Na+ = 140 mEq/L
Cl- = 120 mEq/L
SID = 20 mEq/L
SID
2 liter
 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
SID : 38 
1 liter
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
SID : 19  Asidosis
2 liter
PLASMA + Larutan RINGER LACTATE
Plasma
Ringer laktat
Laktat cepat
dimetabolisme
Na+
= 140 mEq/L
Cl- = 102 mEq/L
SID= 38 mEq/L
1 liter
SID : 38
Cation+ = 137 mEq/L
Cl- = 109 mEq/L
Laktat- = 28 mEq/L
SID = 0 mEq/L
1 liter
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;
Plasma + NaHCO3
asidosis
hiperkloremik
Na+ = 140 mEq/L
Cl- = 130 mEq/L
SID =10 mEq/L
25 mEq
NaHCO3
1 liter
1.025
liter
Na+
HCO3 cepat
= 165 mEq/L dimetabolisme
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
K
HCO3-
SID
HCO3-
Keto-
A-
Na+
SID 
A-
Na+
Cl-
ClLactic/Keto asidosis
Normal
Ketosis
GANGGUAN PD ASAM LEMAH:
Hipo/Hiperalbumin- atau PK
HCO3
SID
K
Na
Cl
Normal
SID
K
HCO3
Alb-/P
Alb-/P-
Na
HCO3
Alb/P 
Na
Asidosis
hiperprotein/
hiperposfatemi
Cl
Acidosis
SID
Alkalosis
hipoalbumin
Cl /hipoposfate
mi
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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