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STEWART APPROACH

In Clinical Setting

Anang Achmadi
Department of Anesthesiology & Intensive Care
Santosa Hospital Bandung Central
BGA/ AGD

•  pH : 7.42

?
•  pCO2 : 35
•  pO2 : 100
•  BE : -2
• HCO3 : 21
GANGGUAN KESEIMBANGAN ASAM BASA
TRADISIONAL

DISORDER pH PRIMER RESPON


KOMPENSASI
ASIDOSIS ↓ HCO3- ↓ pCO2 ↓
METABOLIK
ALKALOSIS ↑ HCO3- ↑ pCO2 ↑
METABOLIK
ASIDOSIS ↓ pCO2 ↑ HCO3- ↑
RESPIRATORI
ALKALOSIS ↑ pCO2 ↓ HCO3- ↓
RESPIRATORI
AKIBAT ASIDOSIS BERAT
Kardiovaskular Respirasi
Gangguan kontraksi otot jantung Hiperventilasi
Penurunan kekuatan otot nafas dan
Dilatasi Arteri,konstriksi vena, dan menyebabkan kelelahan otot
sentralisasi volume darah Sesak
Metabolik
Peningkatan tahanan vaskular paru Peningkatan kebutuhan metabolisme
Resistensi insulin
Penurunan curah jantung, tekanan Menghambat glikolisis anaerob
darah arteri, dan aliran darah Penurunan sintesis ATP
hati dan ginjal
Hiperkalemia
Peningkatan degradasi protein
Sensitif thd reentrant arrhythmia dan
penurunan ambang fibrilasi Otak
ventrikel Penghambatan metabolisme dan
regulasi volume sel otak
Menghambat respon kardiovaskular Koma
terhadap katekolamin

Management of life-threatening Acid-Base Disorders, Horacio J. Adrogue, And Nicolaos EM:


Review Article;The New England Journal of Medicine;1998
AKIBAT ALKALOSIS BERAT
Kardiovaskular
Konstriksi arteri
Penurunan aliran darah koroner
Penurunan ambang angina
Predisposisi terjadinya supraventrikel dan ventrikel
aritmia yg refrakter
Respirasi
Hipoventilasi yang akan menjadi hiperkarbi dan
hipoksemia
Metabolic
Stimulasi glikolisis anaerob dan produksi asam organik
Hipokalemia
Penurunan konsentrasi Ca terionisasi plasma
Hipomagnesemia and hipophosphatemia
Otak
Penurunan aliran darah otak
Tetani, kejang, lemah delirium dan stupor

Management of life-threatening Acid-Base Disorders, Horacio J. Adrogue, And Nicolaos EM:


Review Article;The New England Journal of Medicine;1998
CARA TRADISIONAL

Hendersen-Hasselbalch

The disadvantage of men not


knowing the past is that they do not
know the present.
G. K. Chesterton
Am J Respir Crit Care Med Vol 162. pp 2246–2251,2000
Traditional view
" Problems:
" 1. Which one is the independent variable?
" 2. What is the source of hydrogen ions?
" 3. Does not provide quantitative
assessment
" 4. Does not explain dilutional acidosis or
contraction alkalosis
" 5. Does not explain hypoalbuminemic
alkalosis
Subversive New Concepts
in Acid-base Physiology

" New paradigms are emerging (Current


) in acid base
Opinion Crit Care 1999; 5: 427- 477
physiology
" Based on the work of the late Peter
Stewart (Can J Physiol Pharmacol 1983; 61:
1444-1461)

" They are subversive because they


challenge traditional teaching
Stewart’s Approach

" The Henderson-Hesselbach equation


describes the relationship of 3 linked
variables but does not say which is
dependent and which independent
" The solvent (H2O) not the solutes is
the largest source of hydrogen ions
Menurut Stewart ;

pH atau [H+] DALAM PLASMA


DITENTUKAN OLEH

DUA VARIABEL

VARIABEL DEPENDENT
INDEPENDEN VARIABLES

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


VARIABEL INDEPENDEN

CO2 STRONG ION WEAK ACID


DIFFERENCE

pCO2 Atot
SID
Controlled by
The protein
the respiratory
The electrolyte concentration
system
composition of the (controlled by the
blood (controlled liver and metabolic
by the kidney) state)
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.
MENGAPA DISEBUT ION KUAT DAN LEMAH ?

100
80
70
60
% ter-ionisasi 50 pK
40
30
20
10

2 3 4 5 6 7 8 9

pH
Suatu ion dikatakan kuat atau lemah tergantung dari pKnya (pH, dimana 50%
dari substansi tsb terdisosiasi). Mis; pK Lactate 3.9 (berarti, pada pH normal,
hampir 100% laktat terdisosiasi ). H2CO3 dan Alb disebut asam lemah karena
pada pH normal hanya 50% substansinya terdisosiasi.
STRONG ION DIFFERENCE
Gamblegram
Mg++
Ca++
K+ 4
SID

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


Na+
140 Cl-
102
[Na+] + [K+] - [Cl-] = [SID]
140 mEq/L + 4 mEq/L - 102 mEq/L = 34 mEq/L

KATION ANION
Hubungan SID dgn pH/H+

Konsentrasi H+ [H+] ↑↑ [OH-]


↑↑
SID↓ SID
SID↑
Na Na Na
Cl Asidosis Cl Alkalosis Cl

(–) SID (+)

Dalam cairan biologis (plasma) dgn suhu 370C, SID selalu positif,
nilainya berkisar 30-40 mEq/Liter
PRINSIP UMUM
" Hukum kekekalan massa (Law of Mass):
" Jumlah dari suatu zat/substansi akan selalu konstan
kecuali ditambahkan atau dikurangi dari luar, atau
dibuat/dirusak oleh suatu reaksi kimia.
" Netralitas elektrik (Electroneutrality):
" Semua larutan sejati mempunyai muatan listrik yang
netral, dimana konsentrasi total kation harus sama
dengan konsentrasi anion
Σ iones (+) = Σ iones (-)

Stewart PA. Modern quantitative acid-base chemistry. Can J Physiol Pharmacol 61:1444-1461, 1983.
Konsep larutan encer
(Aqueous solution)
•  Semua cairan dalam tubuh manusia
mengandung air, dan air merupakan sumber [H
+] yang tidak habis-habisnya

•  [H+] ditentukan oleh disosiasi air (Kw), dimana


molekul H2O akan berdisosiasi menjadi ion-ion
H3O+ dan OH-
WEAK ACID

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


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

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


PENILAIAN ANALISA GAS DARAH
MENGGUNAKAN KOMBINASI BASE
EXCESS DAN STEWART
Nilai2 yg diperlukan:
1.  AGD (BE)
2.  Natrium
3.  Klorida
4.  Albumin

Story DA, Bellomo R. Hendersen-Hasselbach vs Stewart: Another Acid-Base


Controversy; Review Article, Crit Care & Shock (2002)2:59-63
BE = (1 - 0.014Hgb) (HCO3 – 24 + (1.43Hgb + 7.7) (pH - 7.4)`

50
PCO2 = 80 40

40
Base Excess/
[HCO3-]

Alkalosis
Metabolik "20 Base Deficit
30
Base Excess"

Normal "
20 Base Defisit"

Asidosis
Metabolik "
10
7.0 7.2 7.4 7.6 7.8
pH
UNMEASURED ANION (UA)
PADA ASIDOSIS METABOLIK

UA = BE – [(efek Na + efek Cl) + efek Alb]


BASE EXCESS DAN STEWART
(a) Free water
n  0.3 x (Na-140)
Jika + à efek alkalinisasi
(b) Chloride effect Jika - à efek asidifikasi
n  102-(Cl x 140/Na)
(c) Albumin effect
n  (0.148 x pH - 0.818) (42-[alb])
n  UA = BE/BD – [(a) + (b) + (c)] mEq/L
Magder S. Pathophysiology of metabolic acid-base disturbances in patients with critical illness.
In: Critical Care Nephrology.Kluwer Academic Publishers, Dordrecht, The Netherlands, 1998. pp 279-296.
Ronco C, Bellomo R (eds).
Clinical Investigations

Strong ions, weak acids and base excess:


a simplified Fencl–Stewart approach to
clinical acid–base disorders
D. A. Story, H. Morimatsu and R. Bellomo . British Journal of Anaesthesia, 2004, Vol. 92,

•  SBE(mmol/l=meq/l);
–  from a blood gas machine
•  Na–Cl effect (meq/l)=
–  [Na+]–[Cl–]–38
•  Albumin effect (meq/l)=
–  0.25x[42–alb(g/l)]
•  Unmeasured ion effect (meq/l)=
–  SBE–(Na–Cl) effect–alb effect
Henderson-Hasselbalch Stewart’s Strong Ion model

SECONDARY/
EFFECT PRIMARY/
CAUSAL
WORKSHOP ACIDBASE
STEWART PERDICI 2006
STEWART APPROACH
Pada Pasien Syok
Statement of the Problem
Endpoint Resuscitation

Traditional Normalization Compensated


Marker of Vital Sign SHOCK
Urine Output

INADEQUATE OXYGENATION

Scalea TM, Maltz S, Yelon J, et al.


Crit Care Med 1994; 22:1610-1615
Acute Hypoperfusion
↑ Blood Lactate
Imbalance between
O2 demand and O2 delivery

MOFS
Anaerobic ? So What?
Inadequate
Cellular
Oxygenation

Inadequate
Anaerobic Lactic Acid
Energy
Metabolism Production
Production

Metabolic Metabolic
Cell Death! Acidosis
Failure
6 Key steps in oxygen cascade
O2
Uptake in the Lung Oxygenation PaO2

Carrying capacity Haemoglobin SaO2 - Ht DO2

Delivery Cardiac Output Flow rate - ø

Organ distribution Autoregulation


Nervous Syst
Diffusion Distance DiffusionHumoral
distance
Local Control

Cellular use Mitochondria


Lactate monitoring in resuscitation
Failure of blood lactate to return to normal following
resuscitation carries a poor prognosis
Blood Lactate (mmol/L) Mortality
<1 18%
2-4 74%
>5 100%

•  Mitochondrial failure due to hypoxia


•  NADH>NAD+
•  Anaerobic glycolysis continues
DEFINISI SYOK
Gangguan dari perfusi jaringan yang terjadi akibat adanya
ketidakseimbangan antara suplai oksigen ke sel dengan
kebutuhan oksigen dari sel tersebut.
Semua jenis shock mengakibatkan gangguan pada perfusi
jaringan yang selanjutnya berkembang menjadi gagal
sirkulasi akut atau disebut juga sindrom shock

IT IS NOT
LOW BLOOD PRESSURE !!!
IT IS HYPOPERFUSION…..
TREATMENT CONCEPT OF SHOCK

ENHANCING PERFUSION / OXYGEN DELIVERY

DO2 = CO x CaO2
Cardiac Arterial O2 content
output
O2 delivery/DO2 = HR X SV X Hb X Sa02 X 1.34 + Hb X PaO2

Fluids
Inotropes Preload Transfuse Partially
Contractility Vasoactive dependent
on FIO2 and
After load pulmonary
status
Content of common IV Fluids
content D5W 0.9% 0.45% 3% LR/ Gela HES 6% SPPS
NaCl NaCl Na Cl Hartman fundin
n’s
Na 154 77 513 130 154 154 130 –
(mEq/L) -- 160
Cl 154 77 513 109 120 154 130 –
(mEq/L
-- 160
K 4 <1
(mEq/L)
-- -- -- -- -- --
Ca
(mEq/L)
-- -- -- -- 3 -- -- --
Osmol 252 308 154 1026 273 274 310 308
arity

pH 3.2-6.5 5.0 5.0 5.0 6.0-7.5 7.1-7.7 4.0-7.0


--
Others Dextro -- Lactate Gelatin Starch Albumin
se 50g
-- -- 28mEq/L 40g/L 50g
60g/L
(Anesth Analg 2001;93:811–6)
Rapid Saline Infusion Produces Hyperchloremic Acidosis
in Patients Undergoing Gynecological Surgery.
(Scheingraber et al.: Anesthesiology 1999, 90)

Saline Lact. Ringer’s


(n = 12) (n = 12)

Time of infusion (min) 135 ± 23 138 ± 20

Volume after 120 min (ml/kg) 71 ± 14 67 ± 18

Estimated blood loss (ml) 962 ± 332 704 ± 447

Urine output (ml) 717 ± 459 1 075 ± 799


Saline Lactated Ringer ’s
0 min 120 min 0 min 120 min

Bicarbonate 23.5 ± 2.2 18.4 ± 2.0 23.3 ± 2.0 23.0 ± 1.1


(mM)

Anion gap 16.2 ± 1.2 11.8 ± 1.4 15.8 ± 1.4 12.5 ± 1.8
(mM)

Chloride 104 115 104 106


(mM)

Scheingraber et al., Anesthesiology 90 (1999)


Replacing 1 Liter of Blood Loss
with Crystalloid (3:1)

Crystalloid Excess chloride


load (mmol)

3 l of NaCl 0.9 % 165

3 l of lactated Ringer’s 27
Lactated Ringer’s
Normal saline

7.50 pH 50 Carbon dioxide


7.45 # # # 46

7.40 42

mmHg
7.35 38

7.30 * 34
*
7.25 * * 30

7.20 26
0 30 60 90 120 min 0 30 60 90 120 min

4 Base excess 3.0 Lactate


#*
# # # 2.5 #* #*
0
2.0 #*
mmol/l

mmol/l
-4 1.5
*
1.0
-8 *
* 0.5
*
-12 0.0
0 30 60 90 120 min 0 30 60 90 120 min

* P<0.05 intragroup Scheingraber et al., Anesthesiology 90 (1999)


# P<0.05 intergroup
Lactated Ringer’s
Normal saline
148

Sodium
120 Chloride #*
#*
#* #* 115 #*
144 #* #*
mmol/l

mmol/l
#*
110
140
105
* *
* *
* 100
136 * *
0 30 60 90 120 min 0 30 60 90 120 min

45 17.5
Calculated SID Prot-
*
40 15
* * *
mmol/l

mmol/l
* #* 12.5 *
#*
35 *
* 10 *
* *
30 *
* 7.5
*
25
0 30 60 90 120 min 0 30 60 90 120 min

* P<0.05 intragroup Scheingraber et al., Anesthesiology 90 (1999)


# P<0.05 intergroup
Conclusions

0.9% saline = (Ab)normal Saline


Reid et al, Clin Sci, 2003
Kasus 1
" Laki2 22 th mahasiswa semester
akhir dibawa oleh temannya ke IGD
dlm kondisi tdk sadar diduga setelah
pesta Miras. 2 orang temannya
meninggal di IGD
" Na : 140/ K : 7,8/ Ca ion : 1,34, Cl :
106/ laktat : 2,30, pt, aptt, fibrinogen
dbn
BGA/ AGD
•  pH : 7,04

?
•  pCO2 : 18
•  pO2 : 136
•  BE : - 30
•  HCO3 : 4,8
•  Sa02 : 97,8
SHUNT %
2-3% 10%
500

400

PaO2 300
20%
200
30%
100
50%
0 21 40 60 80 100
FiO2
Positive effect of Low pH ?

1. Delay the onset of cell death


2. Avoid ongoing tissue hypoxia (shift to the right
of hemoglobin-oxygen dissociation curve)
3. Acidosis during reperfusion limits myocardial
infarct size
4. Correcting the pH took away the protective
effect and accelerated cell death.
Acidic extracellular pH can protect :

" Low pH during reoxygenation after a period


of Anoxia can protect cells from damage.
" If the pHi is restored from <6,5 to >7 during
reperfusion of the heart ,the MPTP
( mitochondria permeability transition pore)
open : an important determinant of
apoptosis.
Halestrap AP et al , 1997, Mol CellBiochem
174:167-172.
OTHER FINDINGS :

1. HCO3 doesn t improve hemodynamic in


critically ill patients who have lactic acidosis
(Cooper; Ann Inter Med. 1990)
2. HCO3 therapy in the treatment of lactic acidosis :
Medicine or toxin?
(Sing Et Al, J Ann. Osteopath. Assoc. 1995)
3. The Routine use of sodium
bicarbonate is no longer recommended.
(In 1992, the American National Conference on
Cardiopulmonary Resuscitation established current
guidelines)
4. CONSENSUS CONFERENCE in FRANCE (June 2000)
organized by The French Reanimation Society
recommend not to give sodium bicarbonate in any
acidosis except in HCO3 loss.
BGA/ AGD hari 2
•  pH : 7,27

?
•  pCO2 : 20,9
•  pO2 : 210,9
•  BE : - 17,3
•  HCO3 : 9,5
•  Sa02 : 99,2
•  K : 4,3
•  Mulai sadar
BGA/ AGD hari 3
•  pH : 7,436

?
•  pCO2 : 30,4
•  pO2 : 126,6
•  BE : - 4,0
•  HCO3 : 20,3
•  Sa02 : 98,6
•  K : 4,0
•  Extubasi à pindah ruangan hari ke 5
Kasus 2
•  Wanita 32 th scoliosis kongenital dibawa
oleh suaminya ke IGD dengan sesak berat
dan lemah
•  Ada riwayat minum obat dari herbalis yg
menyebabkan kencing banyak
•  2 bulan sebelumnya dirawat di ICU krg lbh
3 bln di 2 rmh sakit
•  Trakheostomi sdh tertutup
•  Na : 129/ K : 4,9/ Ca ion : 1,18/ Cl : 83/
Mg : 1,80/ Laktat : 1,70
BGA/ AGD
•  pH : 7,197
•  pCO2 : 124

?
•  pO2 : 156
•  BE : 19,7
•  HCO3 : 47,9
•  Sa02 : 98
Critical Care 2005, 9:184-192
Local Control

Asidosis Alkalosis
Hiperkarbia Hipokarbia
↑ temperature ↓ temperature
↑ 2.3 DPG ↓ 2.3 DPG
Low nutrient High nutrient
↓ PO2 tissue ↑ PO2 tissue

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