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ACID BASE DISORDER

in clinical practice

Erwin Kresnoadi


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INTRODUCTION OF

QUANTITATIVE METHOD OFACID BASE BALANCE

STEWART APPROACH

Warning.!

Most Physician has determined that....

This lecture may be harmful to your mental health.


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The disadvantage of men not

knowing the past is that they do not

know the present.

G. K. Chesterton


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Keseimbangan asam basa

Saya punya hasilastrup, artinya

apa nich..?Who cares

aboutacidbasebalance?


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ASAM BASA..

pH

[H+

]


6/78

Analytic tools used in acid

base chemistry CO2-bicarbonate (Boston) approach

Schwartz, Brackett et al

H-H equation The Base deficit/excess (Copenhagen) approach

1948 Singer-Hasting, Buffer Base (BB)

1958 Siggaard-AndersenBase Deficit/Excess

(BDE) 1960, Hb into calculation, modified Standard Base

Deficit/Excess (SBE)

1977 Van Slyke equation to computed SBE

Has been validated by Schlitic and Morgan


7/78

Analytic tools used in acid

base chemistry

1977, Anion Gap approach

Emmet and Narins

To address the limitation of Boston and Copenhagen

1978, Stewart introduced the physical-chemicalapproach

3 independent variable;

PCO2, SID and weak acid

1993, Stewart-Fencl approach 1998, Anion Gap Corrected

Fencl and Figge

2004, simplified Stewart-Fencl approach

Story DA, Morimatsu et al


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GENERAL PRINCIPLES

Three widely accepted methods are used to analyze and

classify acid-base disorders, yielding mutually compatible

results. The approaches differ only in assessment of the

metabolic component (i.e., all three treat PCO2as anindependent variable):

(1) HCO3-concentration ([HCO-]);

(2) standard base-excess;

(3) strong ion difference (Stewart Approach)

For the most part, the differences among these three

approaches are conceptual; in other words, they differ in

how they approach the understanding of mechanism


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Boston Style

1. HCO3-

Brief historical perspective


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ACID BASE WORKSHOP PERDICI2006

[H

+

] x [HCO

3

-

] = K x [CO

2

]x[H

2

O]

Henderson LJ. Das Gleichgewicht zwischen Sauren und Basen im tierischen Organsimus. Ergebnisse der

Physioogie Biologischen Chemie und Experimentellen Pharmakologie 1909;8: 254325

Henderson, 1908

Discovered buffering power of CO2andapplied law of mass action:

K = [H

+

][HCO

3

-

]/[dCO

2

]

where dCO

2

= dissolved CO

2

)


11/78

Acid Base

Notasi pH diciptakan oleh seorang ahli kimia dari Denmark yaituSoren Peter Sorensen, yang berarti log negatif dari konsentrasi ionhidrogen. Dalam bahasa JermandisebutWasserstoffionenexponent (eksponen ion hidrogen) dandiberi simbol pH yang berarti: potenz(power) of Hydrogen.

1909


12/78

pH = -log[H

+

]

defined by Sorensen

[H+] pH

1 x 10-6 6.0

1 x 10-7

7.0

8 x 10-8

7.1

4 x 10

-8

7.42 x 10

-87.7

1 x 10-8

8.0


13/78

pH = 6.1 + log [ HCO3-

] = KIDNEY0.03 x PCO2 = LUNG

Hasselbalch KA. Die Berechnung der Wasserstoffzahl des Blutes aus der freien undgebundenen Kohlensaure desselben und die Sauerstoffbindung des Blutes als Funktion der

Wasserstoffzahl. Biochemische Zeitschrift 1916; 78: 11244.

1916

Hasselbach:Used Sorensen's terminology for Henderson's equationin logarithmic form:

Hendersen-Hasselbach equation (H-H)


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pH = 6.1 + log [ HCO3-]

0.03 x

1. Change inMetabolic disturbance

2. Change afterRenal compensation forRespiratory disturbance

1. Change inRespiratory disturbance

2. Change afterRespiratory compensation for

Renal disturbance

pCO2


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pH = 6.1 + log

[HCO3-]

pCO2

GINJAL

PARU

BASA

ASAM CO2

HCO3HCO3

CO2

Kompensasi

Normal

Normal


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Diagram Davenport

[HCO

3-]

PCO2= 80 40

20

pH

7.0 7.2 7.4 7.6 7.8

10

20

30

40

50

pH = 6.1 + Ginjal

ParuB

A

C

7.4 / 40 / 24

7.2 / 80 / 30

7.6 / 20 / 18Normal


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pH

Alkalosis Metabolik

pH

Alkalosis Respiratori

pH

Asidosis Respiratori

pH

Asidosis Metabolik

Gangguan asam-basa primer


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Diagnosis menggunakan nilai asam basa serum:Davenport Diagram

[HC

O3-]

PCO2= 80 40

20

pH7.0 7.2 7.4 7.6 7.8

10

20

30

40

50

Henderson- Hasselbalch:

pH = pK + log [HCO3-]

s PCO2Asidosis

Respiratori Alkalosis

Metabolik

Alkalosis

Respiratori

AsidosisMetabolik

pH = 6.1 + Ginjal

Paru

atau,

Normal


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Asidosis Respiratori

[HCO3-]

PCO2= 80 40

20

pH

7.0 7.2 7.4 7.6 7.8

10

20

30

40

50

Asidosis

Respiratori

kompensasi = [HCO3-]

Penyebab:

1) PPOK, Gagal jantung

kronik, bbrp pnykt

paru

2) Obat anestesi

Asidosis

Respiratori

terkompensasi


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Metabolic Alkalosis

[HC

O3-]

PCO2= 80 40

20

pH

7.0 7.2 7.4 7.6 7.8

10

20

30

40

50

Alkalosis

Metabolik

kompensasi =PCO2Penyebab:

1) Intake basa >>

2) Kehilangan asam

(Muntah,

penyedotan lambung)

Alkalosis

Metabolik

terkompensasi


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Metabolic Asidosis

[HC

O3-]

PCO2= 80 40

20

pH

7.0 7.2 7.4 7.6 7.8

10

20

30

40

50

Asidosis

Metabolik

kompensasi = PCO2

Penyebab:

1) Kehilangan basa

(eg. diare)

2) Akumulasi asam

(diabetes, gagal ginjal)

3) Asidosis Tubular Ginjal

Asidosis

Metabolik

terkompensasi


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DISORDER pH PRIMER RESPONKOMPENSASI

ASIDOSISMETABOLIK

HCO3- pCO2

ALKALOSISMETABOLIK

HCO3- pCO2

ASIDOSISRESPIRATORI

pCO2 HCO3-

ALKALOSISRESPIRATORI

pCO2

HCO3-

RANGKUMAN GANGGUANKESEIMBANGAN ASAM BASA

TRADISIONAL


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2. BDE (Base Deficit Excess)&

SBE (Standard Base Excess)

Copenhagen style


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Singer and Hastings, 1948,

Whole blood buffer base (BB), defined as the sum of

bicarbonate [HCO3-] & nonvolatile buffer anions (A-)

The change in BB from "normal" was called delta BB

(BB). This change in BB was an expression of the

metabolic component of an acid-base disturbance

BE (Base Excess)

Singer RB, Hastings AB: An improved clinical method for the estimation of disturbances of theacid-base balance of human blood. Medicine (Baltimore)1948; 27:223-242

Introduced the concept of buffer base [BB]

[BB] = [HCO3-] + [A-]


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Modified Base Excess

ECF includes plasma, red cells, and thesurrounding interstitial fluid. Its where the action

takes place in the body regarding acid-basemovement.

Blood-gas machines calculate SBE as:

Standard Base Excess

SBE = (1 - 0.014Hgb) (HCO324 + (1.43Hgb + 7.7) (pH - 7.4)`


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[HC

O3-]

pCO2= 80 40

20

pH

7.0 7.2 7.4 7.6 7.8

10

20

30

40

50

AsidosisMetabolik

Base deficit;Kekurangan Basa;

Jumlah Basa (HCO3) yg

harus ditambahkan agarpH normal

AlkalosisMetabolik

Base excess;Kelebihan Basa; JumlahBasa (HCO3) yang harus

dikurangi agar pHnormal

Base Excess/Base Deficit

Normal

Base Defisit

Base Excess


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How to determine the

cause of Metabolicacidosis?

Anion Gap

Improve Anion Gap

Strong Ion Gap


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Normal


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Increased anion gap acidosisNormal anion gap acidosis

Na

K Cl

AG

HCO-3

AG = 10-15

25

105145

Normal

Na

K Cl

HCO-3

AG

15

115

145

= 15 (normal)

Na

K

Cl

HCO-3

AG/Other

anion

= 25

15

105

(normal)

145

HCO3-decreases and replaced by Cl-so

there is a Cl-shift :Eg. Diarrhea or

simple gain of H+

HCO3-decreases and replaced by anions

other than Cl-so no Cl-shift: Eg.renal

failure and diabetic keto-acidosis

Metabolic acidosis

HCO3-


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Figge J, Jabor A, Kazda A, Fencl V: Anion gap and hypoalbuminemia. Crit Care Med 1998,26:1807-1810.

Improved Anion Gap ?Anion Gap corrected

AG = pH ((1.16 * alb) + (0.42 * phos)) (5.83 * alb) (1.28 * phos)

1. AG per se is helpful only for discriminating the cause of ametabolic acidosis, diabetic ketoacidosis, lactic acidosis,salicylate, and the like.

2. It is of no value in discriminating the cause of a metabolic

alkalosis because the ions responsible (usually decreased Cl- )are all measured

Schlichtig R, Grogono AW, Severinghaus JW. CURRENT STATUS OF ACID-BASEQUANTITATION IN PHYSIOLOGY AND MEDICINE; Anesthesiology Clinics of North

America. B. Saunders Co. Vol 16, No 1, March 1998


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3. STEWART AND

TRADITIONAL APPROACH(Stewart-Fencl app roach)


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Na+

140

K+ 4Ca++Mg++

Cl-

102

HCO3

A-

Buffer Base= SID = HCO3-+ A-

SID & BASE EXCESS

(expected if pH = 7.4 and pCO2= 40)

Any deviation in [Na+], [Cl-] or [Alb-] from normal values will

produce abase excess or deficit

Cl-

102

A-

HCO3-

BECl (-)

Buffer

Basea

Siggaard-Andersen, Base excess or buffer base (strong ion difference) as a measure of a

non-respiratory acid-base disturbance. Acta Anaesthesiol Scand, 1995

Buffer Basea- Expected Bu ffer BaseBECl=


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SID = Buffer Base

0

20

40

60

80

100

120

140

160

Cations Anions

Na+ Cl-

K+, Mg++, Ca++

mEq/L

Lactate,Other

anions

Cl-

A-

HCO3-

SID BB


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SID = Buffer Base

0

20

40

60

80

100

120

140

160

Cations Anions

Na+ Cl-

K+, Mg++, Ca++

mEq/L

Cl-

A-

HCO3-

SID BB

BaseDeficit


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SID = Buffer Base

The standard base

excess corresponds to

the change in SID

required to restore theplasma (in vivo) to pH

7.40 with pCO2of 40

mm Hg

R2=0.9527

-10

-8

-6

-4

-2

0

2

4

6

-8 -6 -4 -2 0 2 4

A/V SIDe

A/VSBE

Kellum et al. J Crit Care 1997; 12: 7-12


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SBE = SIDex

[SIDex] mEq/L

[S

BE]mEq/L

-30

-20

-10

0

10

20

-30

-20

-10

0

10

20

Schlichtig R. Adv Exper Med Bio. 1997;411:91-95


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The Fencl-Stewart

Formula


47/78

Efek SID

Blood Gas Analysis

Step 1; Base-excess effect of the Na Cl

[(efek Na + efek Cl) + efek Alb]E

UA

= BE

Step 2; Base-excess of the albumin

BE

UA

effect is the residual difference

If there were no abnormalities in

Na,Cl,Alb, or UA anions, then BE would be

equivalent to BE

UA

.

Fencl V, Leith DE: Stewarts quantitative acid-base chemistry:

Applications in biology and medicine. Resp Physiol1993, 91:1--16.


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BEfrom the Blood Gas Machine

SID effect, mEq/l = A + B

A. Free Water effect on Na+

= 0.3 x ([Na+

]

140) B. Corrected Cl-effect

= 102 ([Cl-] x 140/[Na+])

Total weak acids effect, mEq/l

= 0.123 x pH - 0.6310 x (42 - [Albumin])UA effect = BE efSID efATot ef

BASE EXCESS DAN STEWART

Stewart-Fencl, 2000


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BDE adjustment for serum albumin


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Strong Ion Difference inGastrointestinal Tract

1. Magder S. Pathophysiology of metabolic acid-base disturbances in patients with critical illness. In:CriticalCare Nephrology. Kluwer Academic Publishers, Dordrecht, The Netherlands, 1998. pp 279-296.Ronco C,Bellomo R (eds).

2. Sirker AA et al.Acid base physiology: the traditionaland the modernapproaches. Anaesthesia,2002, 57; 348-356

M t h d tSID plasma

l


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WORKSHOP ACIDBASE

STEWART PERDICI 2006

Sekresigaster

Na

ClH+ Cl-

Cl-

Cl-

SID cairan lambung < / (

) ; asam

Antasida: MgOH, CaOH SID

Pancreas

Na+

Empedu

Na+

Na+

SID plasma

Alkalosis

SID plasma -

Asidosis

SID plasma

normal

SID cairan

intestinal normal

Na+

Na+

Na+

Diare: Na loss

Plasma site

Cl

Na

Cl

Na

H+

ClNa

Muntah, penyedotan

Lambung, sekresi EF >>

Cl loss

Cl-

Na+

Absorbsi

Jejunum

Na+

NaCl

normal

Cl-

Na+

Erwin, 2014

Cl-Na+

Na+Cl-

Cl-

Na+


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Volume dan komposisi elektrolit cairan gastrointestinal

24 h vol.(mL)

Na+(mEq/L)

K+(mEq/L) Cl-(mEq/L) HCO3-

SIDSaliva 500-2000 6 25 13 18

Stomach 1000-2000 80 15 115 -20

Pancreas 300-800 140 7.5 80 67.5

Bile 300-600 140 7.5 110 37.5

Jejunum 2000-4000 130 7.5 115 22.5

Ileum 1000-2000 115 5 92.5 27.5

Colon - 60 30 40 -

Miller, 5th ed,2000.


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WORKSHOP ACIDBASE

STEWART PERDICI 2006

24 h vol.

(mL)

Na+

(mEq/

L)

K+

(mEq/

L)

Cl-

(mEq/

L)

HCO3-

SID

Saliva 500-2000 6 25 13 18

Stomach 1000-2000 80 15 115 -20

Pancreas 300-800 140 7.5 80 67.5

Bile 300-600 140 7.5 110 37.5

Jejunum 2000-4000 130 7.5 115 22.5

Ileum 1000-2000 115 5 92.5 27.5

Colon - 60 30 40 -

From Miller, Anesthesia, 5th ed,2000.

Boron & Boulpaep, Medical Physiology,ch 27,

2003.

pH of Body fluidsVolume dan komposisi elektrolitcairan gastrointestinal

R l C ti f


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CO2 pH

H2O OH -+H+Cl-

Na135 Cl

90

HCO330

Na140 Cl

100

HCO3

Normal

Renal Compensation forChronic Respiratory Acidosis

COPD

Na140 Cl

100

HCO3H+ H

+

SID

CO2+ OH HCO3 CO3-2 + H+

SID n

CO2 CO2+ OH HCO3 HCO3

Cl-

Chloride shift

Carbonic anhidrase

Renal & Respiratory Compensation


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Na140 Cl

100

HCO3

BrainStempH Hours

Days

NH3 Sintesis(Ammoniagenesis)

TA

Na140 Cl

100

HCO322

Non Renal

Met Acidosis

Renal & Respiratory Compensationfor non Renal Metabolic Acidosis

H+

Na140

Cl90

HCO322

NH4Cl

RemovalCO2

Hypochloraemia

H+


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A simplified FenclStewart approach


58/78

Strong ions, weak acids and base excess:

asimplified FenclStewart approachtoclinical acidbase disorders

Story, Morimatsu, Bellomo (2004), British Journal of Anaesthesia. Vol. 92,

SBE = from a blood gas machine =

NaCl effect = [Na+][Cl]38 =...

Albumin effect = 0.25 x [42Alb(g/l)] =

UA= SBE (NaCl)effect Albumin effect =


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Interpretation of blood gasresults using combination

the base-excess (BE) withthe Stewart approach (SID)


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SBE = -10

NaCl effect = [Na+

][Cl

]38 = 14011238 = -10 Albumin effect = 0.25 x [4240(g/l)] = 0.5

UA= -10 (-10) 0.5 = -0.5

Kasus 1:

7.25 / 30 / -10 / 14

Na 140; Cl 112; Alb 4.0



Albumin effect = 0.25 x [42Alb(g/l)] = UA= SBE (NaCl)effect Albumin effect =


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Alb


140

150

102

112BE akibat pe

Cl- -10

HCO3-

Na+ Cl-

Alb

7.25 / 30 / -10 / 14

WD/: Asidosis metabolik karena hiperkloremiaCausal: - Pemberian Lar NaCl berlebihan

- Gagal ginjal akutTh/: Batasi NaCl

HD/CRRT

K 2


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Kasus 2:

7.48 / 50 / + 9 / 34

Na 140; Cl 93; Alb 4.2

SBE = +9

NaCl effect = [Na+

][Cl

]38 = 1409338 = 9 Albumin effect = 0.25 x [4242(g/l)] = 0

UA= 9 9 0 = 0


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K 3


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Kasus 3:

7.30 / 27 / -7 / 18

Na 128; Cl 100; Alb 3.0

SBE = -7

NaCl effect = [Na+

][Cl

]38 = 12810038 = -10 Albumin effect = 0.25 x [4230(g/l)] = 3

UA= -7 + 10 3 = 0


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Alb


140

Na+ Cl-

BE akibat Na -7

7.30 / 27 / -7 / 18

WD/: Acidosis metabolik karena hiponatremia

Causal:- hemodilusi- Overload cairan, fase awal shock oligouri

Th: perbaiki shock, inotropik, HD/CRRT

128

Kasus 4 :


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Kasus 4 :

7.42 / 35 / 100 / -2 / 21 ;

Na 140; Cl 102; Alb 1.8

Menurut H-H normal




SBE = -2

NaCl effect = [Na+

][Cl

]38 = 14010238 = 0 Albumin effect = 0.25 x [4218(g/l)] = 6

UA= -2 0 6 = -8


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140

102

HCO3-

24

Alb

Na+ Cl-

hipoalbumin

HCO3-

30.7

SID normal

BE astrup = - 8 + 6 = - 2

HCO3-

22

BE akibat lact - 8UA = - 8BE akibat hipoalb + 6

7.42 / 35 / 100 / -2 / 21

Lactic Asidosis metabolik maskingoleh hipoalbumin


68/78

New calculator of

stewart acidbase


69/78


70/78


71/78

How to interpret acid base disorder


72/78

How to interpret acid base disorderwith quantitative approach

The threeindependent

variable

The UA

Alkalinizing

process

Acidifying

process

The interpretation of

the results

Acidosis Alkalosis

URB-21112


73/78

Soal

Pria 50 th, riwayat DM dgn th/ OAD,

Ditemukan tidak sadar di tempat tidur.

Empat hari sebelumnya os menderita infeksi paru disertai mual

muntah.

Di UGD somnolen, S; 330C, dyspnea, RR 30-35x/mnt,Leukosit; 20.000, GD; 400.

AGD pertama; 6.8 / 12 / 1.8 / -33.1, Na 140, Cl 103, Alb 4.2,

keton darah 32 mmol/L

24 jam setelah th/ insulin, dan pemberian NaCl 0.9 3 L/hari,pasien mulai sadar dan respon, hasil AGD ke 2; 7.23 / 28 / 11.7 /

-13.4. Na 155, Cl 130. Alb 40, KETON 1 mmol

6 8 / 12 / 1 8 / 33 1 N 140 Cl 103 Alb 4 2 k t d h 32


74/78

6.8 / 12 / 1.8 / -33.1, Na 140, Cl 103, Alb 4.2, keton darah 32

24 jam setelah th/ insulin dan pemberian NaCl 0 9 3


75/78

24 jam setelah th/ insulin, dan pemberian NaCl 0.9 3

L/hari, pasien mulai sadar dan respon, hasil AGD ke 2;

7.23 / 28 / 11.7 / -13.4. Na 155, Cl 130. Alb 40, KETON 1

mmol


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Kesimpulan

Dalam keadaan metabolic acidosis, tubuh mempunyaikemampuan homeostasis alkalinizing response:

Rapid response (within minutes):

Ventilasi paru (pCO2), hyperventilation

Late response (within hours and days):

Chloride adjustment with hypochloremic

Albumin adjustment with hypoalbuminemia

Dalam keadaan metabolic alkalosis, tubuh mempunyaikemampuan homeostasis acidifying response:

Rapid response:

Ventilasi paru pCO2, hypoventilation


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KESIMPULAN


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KESIMPULAN

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