PEMANTAUAN ANALISIS GAS DARAH

PADA PASIEN KRITIS DI ICU

Prof Dr dr Made Wiryana, SpAn.KIC.KAO

Analisis Gas Darah merupakan pemeriksaan
yang esensial pada pasien kritis di ICU oleh
karena dapat dipakai tuntunan diagnosis dan
managemen status ventilasi, oksigenasi serta
keseimbangan asam dan basa
 [HCO -] HCO
Normal
GINJAL
BASA
3
HCO 3
3

pH = 6.1 + log Kompensasi

Normal PARU
pCO2
ASAM CO
CO22
 VARIABEL INDEPENDEN

CO2 STRONG ION DIFFERENCE WEAK ACID

pCO2 SID Atot

 CO2

CO2 Didalam plasma berada • Rx dominan dari CO2 adalah rx

dalam 4 bentuk absorpsi OH- hasil disosiasi air
– sCO2 (terlarut) dengan melepas H+.
– H2CO3 asam karbonat • Semakin tinggi pCO2 semakin
– HCO3- ion bikarbonat banyak H+ yang terbentuk.
– CO32- ion karbonat • Ini yg menjadi dasar dari
terminologi “respiratory acidosis,”
yaitu pelepasan ion hidrogen
akibat  pCO2

OH- + CO2  HCO3- + H+

CA
 STRONG ION DIFFERENCE

Definisi:
Strong ion difference adalah ketidakseimbangan muatan
dari ion-ion kuat. Lebih rinci lagi, SID adalah jumlah
konsentrasi basa kation kuat dikurangi jumlah dari
konsentrasi asam anion kuat. Untuk definisi ini semua
konsentrasi ion-ion diekspresikan dalam ekuivalensi
(mEq/L).

Semua ion kuat akan terdisosiasi sempurna jika berada didalam

larutan, misalnya ion natrium (Na+), atau klorida (Cl-). Karena
selalu berdisosiasi ini maka ion-ion kuat tersebut tidak
berpartisipasi dalam reaksi-reaksi kimia. Perannya dalam kimia
asam basa hanya pada hubungan elektronetraliti.
Gamblegram
Mg++
Ca++
K+ 4 HCO3-
24 SID
Weak acid
(Alb-,P-)

Na+
140
Cl-
102

KATION ANION
SKETSA HUBUNGAN ANTARA SID,H+ DAN OH-

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

Asidosis Alkalosis

(–) SID (+)

Dalam cairan biologis (plasma) dgn suhu 370C, SID hampir

selalu positif, biasanya berkisar 30-40 mEq/Liter
KEKURANGAN AIR - WATER DEFICIT
Diuretic
Diabetes Insipidus
Evaporasi

Plasma Plasma

Na+ = 140 mEq/L

Cl- = 102 mEq/L
SID = 38 mEq/L 140/1/2 = 280 mEq/L
102/1/2 = 204 mEq/L
1 liter ½ liter
SID = 76 mEq/L

SID : 38  76 = alkalosis
ALKALOSIS KONTRAKSI
 KELEBIHAN AIR - WATER EXCESS

Plasma

1 Liter 140/2 = 70 mEq/L

Na+ = 140 mEq/L H2O 102/2 = 51 mEq/L
Cl- = 102 mEq/L SID = 19 mEq/L
SID = 38 mEq/L 1 liter 2 liter

SID : 38  19 = Acidosis
ASIDOSIS DILUSI
GANGGUAN PD SID: Pengurangan Cl-

Plasma

Na+ = 140 mEq/L

Cl- = 95 mEq/L
SID = 45 mEq/L
2 liter

SID  ALKALOSIS

ALKALOSIS HIPOKLOREMIK
 GANGGUAN PD SID:
Penambahan/akumulasi Cl-

Plasma

Na+ = 140 mEq/L

Cl- = 120 mEq/L
SID = 20 mEq/L 2 liter

SID  ASIDOSIS

ASIDOSIS HIPERKLOREMIK
 PLASMA + NaCl 0.9%

Plasma NaCl 0.9%

Na+ = 140 mEq/L Na+ = 154 mEq/L

Cl- = 102 mEq/L Cl- = 154 mEq/L
SID = 38 mEq/L 1 liter SID = 0 mEq/L 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

Cation+ = 137 mEq/L

Na+ = 140 mEq/L Cl- = 109 mEq/L
Cl- = 102 mEq/L Laktat- = 28 mEq/L
SID= 38 mEq/L 1 liter 1 liter
SID = 0 mEq/L

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 2 liter
SID = 34 mEq/L

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

 UA = Unmeasured Anion:
Laktat, acetoacetate, salisilat, metanol dll.

K K HCO3- SID 
HCO3- SID
Keto-

A- A-

Na+ Na+

Cl- Cl-
Lactic/Keto asidosis

Normal Ketosis
Regulation of Acid-Base Balance
Regulatory mechanisms are very sensitive to
small changes in pH
Buffers
Respiratory System
Renal System
 Regulation of Acid-Base Status:
Buffers
• Immediately combine with excess acid to form
substances that do not greatly affect pH.
• Bicarbonate (HCO3-)
– Most important buffer
– Absorption, excretion, production regulated by kidney
• Other buffers: Phosphate, Ammonium, Protein
 Regulation of Acid-Base Status:
Respiratory System
• Increased CO2 or H+ levels => stimulates respiratory =>
increased ventilation => blows off (exhales) CO2=>
eliminating excess acid. If acidotic
• Hyperventilation => CO2 eliminated => improvement in acidotic
state
• If alkalotic (low CO2 or H+):
• hypoventilation => CO2 retained => improvement in alkalotic state
• Quick response: within 1-2 min of pH imbalance
 Regulation of Acid-Base Status:
Renal System
• Kidneys conserve and/or eliminate H+ and
HCO3- in response to abnormal pH
– If acidotic => eliminate H+ (acid) and retain HCO3-
(base) in effort to normalize pH
– If alkalotic => Eliminate HCO3- (base) in effort to
normalize pH
• Response to abnormal pH is slow (hours to
days)
 Regulasi Ph dan mekanisme kompensasi

Rapid regulation (short- Chronic control (long-

term) term)
 Acid Base Imbalances
Respiratory Acidosis
• Acidosis is due to hypoventilation
• Causes:
– COPD (Emphysema, bronchitis)
– failure of respiratory muscles (ALS, Guillain-Barre)
– airway obstruction (e.g., post-op)
• Metabolic compensation: Kidneys excrete H+/retain
HCO3- (if problem lasts hours/days)
 Acid Base Imbalances
Respiratory Alkalosis
• Acidosis is due to hyperventilation
• Causes
– anxiety (Rx with paper bag)
– pneumonia
– pulmonary edema
• Metabolic compensation: Kidneys excrete HCO3-
( if problem lasts hours/days )
 Acid Base Imbalances
Metabolic Acidosis
• Acidosis is due increase in metabolic acids and/or loss of
HCO3-
• Increased acids due to
– diabetic ketoacidosis
– renal failure (kidneys cannot excrete H+)
– poisoning
• Lost alkali (base) due to:
– severe diarrhea
– intestinal malabsorption
• Respiratory compensation: hyperventilation (blow off CO2)
 Acid Base Imbalances
Metabolic Alkalosis
• Alkalosis is due to elevated HCO3- secondary to
loss of acid/H+ or excess alkali intake.
– Loss of acid
– Vomiting
– gastric suction
– diuretics
• Minimal respiratory compensation b/c hypoxemia
will result and stimulate respirations
 ABG Parameters
• PaO2
– Partial pressure of O2
– Normal: 80 - 100 mmHg
– Measures the effectiveness of the lungs in oxygenating the blood.
Reflects ability of lungs to diffuse inspired oxygen across the alveolar
membrane into the circulating blood

• SaO2
– Oxygen saturation
– Normal: > 95%
– % of hemoglobin that is saturated with oxygen.
 ABG Parameters
• PaCO2
– Partial Pressure of CO2
– Normal: 35 - 45 mmHg
– Reflects effectiveness of ventilation (movement of air into
and out of lungs).
• HCO3 –
– Normal: 22 - 26 mEq/l
– Bicarbonate ion; metabolic parameter.
– Part of buffer system.
• pH - Normal 7.35 - 7.40
– Measures acidity
– Determined by relative concentrations of CO2 and
HCO3
• Base Excess
– + 2 mEq/L
– Amount of acid or alkali needed to titrate 1 L of
fully oxygenated blood to a pH of 7.40 when T =
37 & PaCO2 = 40 mm Hg
 ABG Interpretation: Oxgenation
Step 1
• Look at PaO2 and SaO2
– Normal?
– Hypoxemic
 ABG Interpretation:
Assess Acid-Base Balance
Step 2
• Look at pH
– Acidotic, alkalotic, or normal?
– If normal
• High normal?
• Low normal?
 ABG Interpretation:
Assess Acid-Base Balance
Step 3
• Look at PaCO2
– Is it altered (i.e. increased or decreased)?
– If altered, consider the direction of the
alteration:
• Could it have caused the alteration in pH?
• Could it be compensation?
 ABG Interpretation:
Assess Acid-Base Balance
Step 4
• Look at HCO3-
– Is it altered (i.e. increased or decreased)?
– If altered, consider the direction of the
alteration:
• Could it have caused the alteration in pH?
• Could it be compensation?
 ABG Interpretation:
Assess Acid-Base Balance
Step 5
• Decide if the abnormal pH is caused by the
pCO2 (respiratory causes) or the HCO3
(metabolic causes).
 ABG Interpretation:
Assess Acid-Base Balance
Step 6
• Determine if compensation is present
– Look at parameter (PaCO2 or HCO3) that did not
cause the pH disturbance. Has it changed in
effort to normalize the pH?
• If yes, compensation is present.
• If no, compensation is not present.
 Is there appropriate compensation?
Is it chronic or acute?
 Respiratory Acidosis
 Acute (Uncompensated): for every 10 increase in pCO2 -> HCO3 increases by 1
and there is a decrease of 0.08 in pH
 Chronic (Compensated): for every 10 increase in pCO2 -> HCO3 increases by 4
and there is a decrease of 0.03 in pH
 Respiratory Alkalosis
 Acute (Uncompensated): for every 10 decrease in pCO2 -> HCO3 decreases
by 2 and there is a increase of 0.08 in PH
 Chronic (Compensated): for every 10 decrease in pCO2 -> HCO3 decreases by
5 and there is a increase of 0.03 in PH

 Partial Compensated: Change 1 4

in pH will be between 0.03 to
0.08 for every 10 mmHg 10
change in PCO2
2 5
EXPECTED CHANGES IN ACID-BASE DISORDERS

Primary Disorder Expected Changes

Metabolic acidosis
Metabolic alkalosis
Acute respiratory acidosis
Chronic respiratory acidosis
Acute respiratory alkalosis
Chronic respiratory alkalosis
PCO2 = 1.5 × HCO3 + (8 ± 2)
PCO2 = 0.7 × HCO3 + (21 ± 2)
delta pH = 0.008 × (PCO2 - 40)
delta pH = 0.003 × (PCO2 - 40)
delta pH = 0.008 × (40 - PCO2)
delta pH = 0.003 × (40 - PCO2)

From: THE ICU BOOK - 2nd Ed. (1998) [Corrected]

 Calculate the anion gap (AG)
• AG used to assess acid-base status esp in D/D of met acidosis
•  AG &  HCO3- used to assess mixed acid-base disorders

 AG based on principle of electroneutrality:

– Total Serum Cations = Total Serum Anions
– Na + (K + Ca + Mg) = HCO3 + Cl + (PO4 + SO4
+ Protein + Organic Acids)
– Na + UC = HCO3 + Cl + UA
– Na – (HCO3 + Cl) = UA – UC
– Na – (HCO3 + Cl) = AG
 Normal =12 ± 2
 AG corrected = AG+2.5(4-Albumin)
 Acid base disorders

Respiratory acidosis

PH PCO2 HCO3
↓ ↑ ------
 Respiratory alkalosis

PH PCO2 HCO3
↑ ↓ ------
 Metabolic acidosis

PH PCO2 HCO3
↓ ------ ↓
 Metabolic alkalosis

PH PCO2 HCO3
↑ ------ ↑
 Compensation
• The respiratory and metabolic system works
together to keep the body’s acid-base balance
within normal limits.
• The respiratory system responds to metabolic
based PH imbalances in the following manner:
* metabolic acidosis: ↑ respiratory rate and depth
(↓PaCO2)
* metabolic alkalosis: ↓ respiratory rate and depth
(↑PaCO2)
• The metabolic system responds to respiratory
based PH imbalances in the following manner:
*respiratory acidosis: ↑ HCO3 reabsorption
*respiratory alkalosis: ↓HCO3 reabsorption
 Respiratory acidosis
Phase PH PaCO2 HCO3
UNCOMPENSATED ↓ ↑ ------

Because there is no response from the kidneys yet to

acidosis the HCO3 will remain normal
Phase PH PaCO2 HCO3
PARTIAL COMPENSATED ↓ ↑ ↑

The kidneys start to respond to the acidosis by increasing

the amount of circulating HCO3

Phase PH PaCO2 HCO3

FULL COMPENSATED N ↑ ↑

PH return to normal PaCO2 & HCO3 levels are still high to

correct acidosis
 Respiratory alkalosis
Phase PH PaCO2 HCO3
UNCOMPENSATED ↑ ↓ ------

Because there is no response from the kidneys yet to

acidosis the HCO3 will remain normal
Phase PH PaCO2 HCO3
PARTIAL COMPENSATED ↑ ↓ ↓

The kidneys start to respond to the alkalosis by

decreasing the amount of circulating HCO3

Phase PH PaCO2 HCO3

FULL COMPENSATED N ↓ ↓

PH return to normal PaCO2 & HCO3 levels are still low to

correct alkalosis
 Metabolic acidosis
Phase PH PaCO2 HCO3
UNCOMPENSATED ↓ ------- ↓

Because there is no response from the lungs yet to

acidosis the PaCO2 will remain normal
Phase PH PaCO2 HCO3
PARTIAL COMPENSATED ↓ ↓ ↓

The lungs start to respond to the acidosis by decreasing

the amount of circulating PaCO2

Phase PH PaCO2 HCO3

FULL COMPENSATED N ↓ ↓

PH return to normal PaCO2 & HCO3 levels are still low to

correct acidosis
 Metabolic alkalosis
Phase PH PaCO2 HCO3
UNCOMPENSATED ↑ ------- ↑

Because there is no response from the lungs yet to

alkalosis the PaCO2 will remain normal
Phase PH PaCO2 HCO3
PARTIAL COMPENSATED ↑ ↑ ↑

The lungs start to respond to the alkalosis by increasing

the amount of circulating PaCO2

Phase PH PaCO2 HCO3

FULL COMPENSATED N ↑ ↑

PH return to normal PaCO2 & HCO3 levels are still high to

correct alkalosis
TERIMA KASIH