Notiuni fundamentale in EAB

SUUB

EAB

1. Notiuni fundamentale

2. Factori etiologici

-- mecanisme fiziopatologice

-- diagnostic diferential si pozitiv

-- tratament specific

3. Tratament general (nespecific)

Notiuni fundamentale1. Acizi si baze – definitii

2. pH, activitatea H+

3. Electroliti, non-electroliti, ioni, strong ions, weak ions

4. pH-ul extracelular si intracelular

5. Sistemele tampon (buffer)

6. Buffering extracelular si intracelular

7. EAB in tesuturi specifice: SNC, plamani, rinichi

8. Definirea, clasificarea, dinamica tulburarilor acido-bazice primare, secundare, mixte convergente si divergente

9. Evaluarea tulburarilor EAB

10. Efecte sistemice si locale ale tulburarilor EAB

pH-ul neutru

Sol acida → [H+] > [OH

-]

Sol alcalina → [H+] < [OH

-]

Sol neutra → [H+] = [OH

-]

Apa pura (25°C): Kw=10 -14 = [H

+] x [OH

-]

[H+]=[OH

-], pH=7

Apa pura (37°C): pH=6,68 – pH neutru (H

+=OH

-)

pH-ul neutru

pH intracelular vs extracelular

Spatiul extracelularpH=7,4 – alcalin in

termeni absoluti

Spatiul intracelularComparativ cu cel extracelular –pH acid, poate fi alcalin sau acid

in termeni absoluti

EC pH este un surogat pentru IC pH

Spatiul extracelular

Ox

OzOy

CzCy

Cx

Definitii – acizi si baze

ACID

CLASIC ARRHENIUS BRONSTEAD -LOWRY

LEWIS USANOWICH

AcruTurnesol albastru-rosu

Produce gaz inflamabil

cand reactioneaza cu anumite

metale

In solutie apoasa disociaza si elibereaza H

+

Donor de H+

CO2 ?Accepta o pereche de e-

Donor de cationi sau acceptor de anioni

STEWARTAcidul = ceva ce duce la cresterea H

+ a solutiei. Ex. Cl-

Definitii – acizi si baze

BAZA

CLASIC ARRHENIUS BRONSTEAD -LOWRY

LEWIS USANOWICH

AmaraTurnesol albastru-rosuAsemanatoare cu sapunul la atingere

In solutie apoasa disociaza si elibereaza OH

-

Acceptor de H+

Donor depereche de e-

Donor de anioni sau acceptor de cationi

STEWARTBaza = ceva ce duce la scaderea conc. H

+ a solutiei. Ex:

Na,K,Ca,Mg

Electroliti, non-electroliti, ioni

Electroliti + Nonelectroliti

Electrolitii disociaza in ioni

NONVOLATILI

Albumina

Fosfatii

VOLATILI

CO2

Ioni slabi (weak ions – buffer ions) partial disociati

Ioni puternici (strong ions)total disociati

Nu sunt ioni si nu disociaza in ioni. Participa la osmolaritate dar nu si la

puterea ionica a solutiei

STRONG

ANIONS

Cl

Lactat

STRONG

CATIONS

Na

K

Ca

Mg

Totul este relativ ……

Buffer eficient ⇒ pKa ε [pH-1,5 ; pH+1,5]

pK5,9

pK8,9

Buffer ionsStrong ions Strong ions

Totul e relativ…

Generarea acizilor

PlamanF

ACO2=VCO2/VA

HCO3 filtr=GFR x HCO3pHCO3 filtr=180L/zi x 24 mmol/L

= 4320 mmol/24 h

Grad H+= x 1000pHmin=1,5

50-100 mEq acizi ficsiE x cr/zi� 300 mEq/zi

Rinichi

H2CO3CO2 (volatil) VCO212 moli+20 moli/24hAdica 716,8 l/24 h STP

Metabolism protidic

Metabolism glucide si lipide

non - H2CO3

90% reabs in TCP

10% in TCD

Interventia sistemelor tampon

intra si extracelular

Acidoza metabolica acuta

57% TIC (+OS) 43% TEC

Alcaloza metabolica acuta

32% TIC (+OS) 68% TEC

Acidoza respiratorie acuta

97% TIC (Hb) 3% TEC

Alcaloza respiratorie acuta

99% TIC (Hb) 1% TEC

Raspunsul mecanismelor compensatorii in ACM si ALM

Sisteme buffer (tampon) – CLASIC!Def: Solutie ce se opune modificarii pH-ului

propriu la adaosul unui acid sau bazeacid slab +sarea sa alcalina

baza slaba + sarea sa acida

Buffering in ECF Buffering in sange

Buffering in ICF Buffering in urina

B. MAJOREHCO3/CO2

B. MAJOREHCO3/CO2Hemoglobina

B. MAJOREproteine (gr. )fosfati

B. MAJORENH3/NH4+

fosfati

B. MINOREproteine (HA/A)↓↓

fosfati (HPO42-/H2PO4-)

B. MINOREproteinefosfati

B. MINOREHCO3/CO2

β sistem tampon (inchis)

TB=B- + HB

pH= - log H+

pK= - log Ka

Pt H+=K ⇒ B-=HB si β =2,3 x =max

Concluzii:

1. β ↑ cu ↑TB

2. β=max cand pKa∼pH (Ka=H)

3. Eficienta maxima pt pKa=pH±1,5

TB

4

HB⇔H++B-

HCl

Sistem tampon (inchis)

Sisteme tampon sangvineHCO3/CO2d

- β=55 mEq/unit pH (la pH=7,4)

- sistem tampon deschis, simplu

- β=2,3 x HCO3 (fara max, min)

Non HCO3/CO2d

- sistem tampon inchis, multiplu

- hemoglobina + proteine + fosfati

- βmax=25 mEq/unitate pH

- βnon-Hb=5 mEq/ unitate pH

pK non ∼7,4 ⇒ Ka=H+ si β=max la pH=7,4

βmax=25=(2,3 x TB)/4

TB=B-+HB

B-=HB

B-=HB=21,73mEQ

Sisteme tampon sanguine HCO3/CO2

inchis vs deschis

Constanta BunsenDef: CS (coeficientul de solubilitate – absorbtie al gazului intr-un lichid, la Tx) =

cantitatea de gaz ce poate fi absorbita (“dizolvata”) de 1ml de lichid, la

pgaz=760mmHg. Variaza invers proportional cu T

Ex: pentru CO2, CS=0,57 ml/ml plasma la 37°C, p=760 mmHg

PV=νRT

T=310K Vμ=25,7 l/mol

P=1 atm

R=8,3142x103J/kmolxK

Constanta Bunsen= x 1000x =0,03 mmol/l pt 1 mmHg

Ex: pt pCO2=40 mmHg la 37 grade sunt 0,03x40=1,2 mmoli CO2/l Plasma

0,57ml/ml lichid

25,7 ml/mmol 760

1

Ecuatia Henderson - Hasselbach

Buffer slab aparent

K1 K2 K3

Definitiile tulburarilor EAB

ACIDOZA

- Proces anormal ce ar

duce la ↓pH daca nu ar

exista fenomen

secundar ca raspuns la

modificarea primara

ALCALOZA

- Proces anormal ce ar

duce la ↑pH daca nu ar

exista fenomen secundar

ca raspuns la modificarea

primara

TULB EAB MIXTE

- 2 sau mai multe

tulburari primare

TULB EAB SIMPLE

- Un singur proces

primar ± compensare

in desfasurare

ACIDEMIE

Arterial: pH<7,36

(H+>44nM)

ALCALEMIE

Arterial: pH>7,44

(H+<36 nM)

Acidoza metabolica si alcaloza metabolica (IN VITRO)

pCO2=40mmHgCO2d=1,2 mmoliSaO2=100%; T=37 CHb=150 g/l

H+

0,00004

mmoli

B-

21, 73

mmoli

HCO3-

24

mmoli

HB

21,73

mmoli

1L

HB

21,73

mmoli

B-

21,73

mmoli

H+

0,00004

mmoli

HCO3-

24

mmoli

1L

+x

-z

-y

+z

10 Cl

x+y+z=10 mmoli HClx=0,000015y=6,6z=3,4

10 mmoli

HCl

yCO2

x+y+z=10 mmoli NaOHx=0,000009y=7,1Z=2,9

10 Na

-x

-z+z

+y

10 mmoliNaOH

y CO2

yH+ + yHCO3

Acidoza metabolica si alcaloza metabolica (IN VITRO)

NBB=HCO3N+BN=45,73 mmoli NBB=HCO3N+BN=45,73 mmoli

PBB=HCO3p+BP=NBB-y-z PBB=HCO3p+BP=NBB+y+z

BE=∆BB=-y-z=-10 mmoli BE=∆BB=y+z=10 mmoli

pH actual < pHN pH actual > pHN

pH standard = pH actual pH standard=pH actual

HCO3 standard=HCO3 actual=HCO3N -y HCO3 standard=HCO3 actual=HCO3N +y

Acidoza respiratorie si alcaloza respiratorie (IN VITRO)SaO2=100%T=37C; Hb=150mg/dlPCO2=40 mmHgCO2d=1,2 mmoli

H+

0,00004

mmoli

B-

21, 73

mmoli

HCO3-

24

mmoli

HB

21,73

mmoli

1L

HB

21,73

mmoli

B-

21,73

mmoli

H+

0,00004

mmoli

HCO3-

24

mmoli

1L

+x

-y

+x+y

+y

x=0,00002555 mmoliy=5,26 mmoli

x=0,0000148 mmoliy=4,94 mmoli

-x

-y+y

-x-y

PCO2=80 mmHgCO2d=2,4 mmoli

x+yx+y

x

y

PCO2=20 mmHgCO2d=0,6 mmoli

x+y

x+y

xy

Acidoza respiratorie si alcaloza respiratorie (IN VITRO)

NBB=HCO3N+BN=45,73 mmoli NBB=HCO3N+BN=45,73 mmoli

PBB=HCO3p+BP=NBB+x ≅45,73 PBB=HCO3p+BP=NBB-x ≅45,73

BE=∆BB=0 BE=∆BB=0

pH actual < pHN pH actual > pHN

pH standard = pHN pH standard=pHN

HCO3 standard=HCO3N HCO3 standard=HCO3N

HCO3 actual=HCO3N +x+y HCO3 actual=HCO3N –x-y

Diagramele Davenport

Diagrame Davenport

METABOLIC ALKALOSIS

Diagrame Davenport

Diagrame Davenport

Acidoza respiratorie IN VIVO-IN VITRO

ISF

CO2+H2O

H2CO3

HB

HCO3-

BLOOD

+B-

+

AC

y-z

HCO3-

z

CO2+H2O

H2CO3

HB

HCO3-

BLOOD

+B-

+

AC

y

IN VIVO IN VITRO

Acidoza respiratorie IN VIVO-IN VITRO

PARAMETRU IN VITRO IN VIVO

HCO3 actual y <

BB N < sau N

BE 0 < sau 0

pH st N < sau N

HCO3 st N < sau N

Base Excess(BE)-To BE or not to BE?

BOSTONTUFTS UNIVERSITY

SCHWARTZ, BRACKETT,

RELMAN

CO2/HCO3 approach

COPENHAGASIGGAARD-ANDERSON

Base deficit/excess approach

SAN FRANCISCOSeveringhaus

Base deficit/excess approach

The Great Transatlantic

Debate (1960→)

Base Excess (BE) – To BE or not to BE?PARAMETRU ABREVIERE DEFINITIE

Buffer Base BB HCO3-+Alb-+Hb-

Delta Buffer Base ∆BB PBB-NBB

Base Excess in blood sauActual Base Excess

cBase(B) sauABE

mEq de acid puternic/baza tare necesari titrarii sangelui la pH=7,4 (conditii: pCO2=40mmHg, T=37C, SaO2=actuala/100%)

Base Excess in ECF sauStandard Base Excess sauBase Excess in vivo

cBase(ecf) sauSBE

BE al unui model ECF – sg 1/3 + 2/3 ISF (Hb=5 g/dl=3mmol/l)

SBE=0,9287 [HCO3- - 24,4+14,83 (pH-7,4)]

BE(van Slyke)={ [HCO3- ]- 24,4+(2,3Hb+7,7)(pH-7,4)} x (1-0,023Hb)

Hb—mmol/l

Base Excess(BE)-To BE or not to BE?

BOSTON-Hendersson- Haseelbach-HCO3 si CO2- variabile

independente (?)-6 tulburari AB, 6 ecuatii-eficienta in tulb. simple-“oarba” la pacientul critic (tulb mixte)-ACM HCl vs ACM NCl ?

COPENHAGA1948 – Singer si Hastings�BB�ABB1950 – Astrup(Copenhaga)�echilibrarea sg la pCO2 anume1960- Siggaard-Andersen� BEblood,

nomograma1963-Sigaard-Andersen� SBE

-Abordare eficienta in tulb simple dar “oarba” la pacientul critic-ACM HCl vs ACM NCl?

BOSTON

WINTERS

BOSTON

Old COPENHAGA

-sisteme de coordonate pH-log pCO2-echilibrare sange cu doua “gaze” cu continut diferit si stiut de CO2 (deci pCO2 cunoscut) + masurare pH-construire linie pH-log pCO2-citire BB, BE actual, HCO3 st, pCO2 actual

COPENHAGA

Bicarbonatul actual vs standard

Acidoza respiratorie ± proces metabolic

Factor metabolic

HCO3-ul obtinut = standard (pCO2=40)

Analiza a probei pentru HCO3

proba sange

Alcaloza respiratorie ± proces metabolic

proba sangeHCO3 actual

Factor respirator

HCO3 actual+++

HCO3 standard+

HCO3 actual++++

HCO3 standard++++

pCO2=40pCO2=40

Gap-ul anionic (Anion Gap)

-Emmett si Narins (1977) “salveaza” Boston-ul si Copenhaga- Legea electroneutralitatii (in plasma): suma ionilor pozitivi (ωi) este egala cu suma ionilor negativi (σi )

UM ωi+

Na+

K+

UM σi-

HCO3-

Cl-

Cel mai frecvent masuram

Na+ , K+ HCO3-, Cl-

AG=(Na++K+)-(Cl-+HCO3-)? N=7-17 mEq/l

INTERVAL PREA MARE

AG=UM σi- - UM ωi

+

GAP-ul anionic – Ce au presupus?

AG=Na+ + K+ - Cl- -HCO3-

AG – A-tot – UMsp = 0

A-tot = A tot x 0,9

A tot = 2,4 x Prot pl g/dl (in mEq/l)A-

tot = Prot pl x 2,4 x 0,9A-

tot = 13,6 – 16,8 mEq

AG = 7-17 mEq/l

Gap-ul anionic – Ce au presupus?

(Na + K)-

(Cl + HCO3)

(Na + K)-

(Cl + HCO3)

(Na + K)-

(Cl + HCO3)

+yHCl (-y NaHCO3)

∆AG=0

+yHCl + zHX +y H+X-

∆AG=+y∆AG/ ∆HCO3=1

∆AG=zBE=-y-z

In realitate…

ECFECF

HCO3i- (9/10 x ½ c)HCO3i- (9/10 x ½ c)

B-i(1/10 x ½ c)B-i(1/10 x ½ c)

Nai, KiNai, Ki

ICF

c H+X-c H+X-

c/2 H+

c/2 Na+/K+

+ ERITROCIT

GAI=Nai+Ki – Cli-HCO3i

ptr X-=L-

GA=Nai+Ki + c/2 Na/K-Cli - HCO3i+9/20c HCO3

∆GA= 19/20 c (<c)

ptr X-=Cl-

GA=Nai+Ki + c/2 Na/K-Cli-cCl-HCO3i+9/20c HCO3

∆GA= -c/20 (<0)

In Ac HCl GA este N dar mai < GAI

∆GAI / ∆ HCO3=19c/20 x 20/9c=2,1

Gap-ul anionic (Anion Gap)

AG↑AG↓

ωi+ ↑(nu Na,K)

-↑Ca2+, Mg2+

-↑Li-↑Ig G

σi- ↓(nu Cl,HCO3)

- hipoalbuminemie

- pH ↓

Eroare laborator

-Bromism (↑Cl) -Hiperlipidemie (↑Cl)

σi- ↑(nu Cl,HCO3)

-Hiperalbuminemie-Ph ↑-↑σi anorganici

- fosfat- sulfat

-↑σi organici- L-lactat- D-lactat- Ketone (DZ,

Alc, inanitie)- uremie

-Toxice- salicilati- paraldehida- metanol, formaldehida- format- etilenglicol-

glicolat, oxalat- toluen

-Anioni neidentificati (critically ill pacients)

- toxine- uremie- rabdomioliza

(+fosfat)- “stress acidosis”

(ciclul Krebs?)

ωi+ ↓ (nu Na,K)

- ↓ Ca2+, Mg2+

Cauze de acidoza cu GAP N si ↑

AG=N AG= ↑

Pierdere intestinala de HCO3 (UAG - )- diaree-fistule pancr, biliare, intest- ureterosigmoidostomie

(schimb Clur – HCO3 col)

Cetoacidoza-DZ- alcoolism- inanitie

Pierdere renala de HCO3- RTA 2 (proximala) (UAG variabil)- acetazolamida (UAG+)- catoacidoza (tratament)- posthipocapnie cronica)

Acidoza lactica- L-lactat (A+B) (L/P↑; L/P N)- D-lactat

Defect de excretie H+ renal (NH4+)-RTA 1 (distal, K ↓)- RTA 4 (K ↑)

Toxice- etilenglicol- metanol - salicilati- toluen - paraldehida

Diverse- hiperalimentatie cu aa+Cl-

- administrare HCl in ALC met

GAP-ul anionic si limitele sale

1. Acidoza/alcaloza respiratorie fara raspuns renal il modifica (vezi

model� la pCO2=80 mmHg, in vitro, ∆AG < 0 pe seama B

nonHb)

2. Acidoza “dilutional” GAP↓(SID ↓, Na↓, Na/Cl=N) si alcaloza “concentrational” GAP ↑ (SID ↑, Na ↑, Na/Cl=N)

3. Presupunerile autorilor nu sunt valabile la pacientul critic

AGadj=AG+0,25(40-Alb); N=7-17mEq/L; Alb=g/L

AGcor=AG-(0,2 x Alb+1,5 x P); N<5mEq/L; P=mmol/LAGcor=AG-Alb x (0,123 x pH-0,631) - Pix(0,309 x pH-0,469)

AGcor=AG-(0,28 x Alb+1,8 x P); N<5mEq/L; P=mmol/LAGcor=AG-(0,28 x Alb+0,6 x P); P=mg/dl

Raportul delta/delta (∆AG/ ∆HCO3)

Ce au presupus?

1. ∆H+= ∆HCO3

2. pentru H+X-: SD(H+)=SD(X-)

In realitate:

1. ∆H+ >∆HCO3

2. pentru H+X-: SD(H+) >>SD(X-)

Observatii:

1. care e val N a AG? (7-17- ∆mare)

2. folositi AGadj (nu AGcor)

3. ∆/ ∆, AG,BE prezinta aceeasi “mutatie” autosomal dominanta

∆/ ∆>1 ⇒+ALC. M∆/ ∆=1 ⇒ AC. M cu X-

∆/ ∆ < 1 ⇒ +AC.M HCl

1< ∆/ ∆ ≤ 2 ⇒AC. M cu X-

∆/ ∆ ≤1 ⇒ +AC. M HCl∆/ ∆>2 ⇒ +ALC. M

UAG (gap-ul anionic urinar)

GAP-ul anionic urinar

Anioni in urina:HCO3ClPO4SO4 Anioni organici

MasuratiCl

Cl + UA = Na +K +UC

UAG = Na+ K –Cl = UA -UC

Cationi in urina:NaKMgCaNH4

NemasuratiHCO3PO4SO4Anioni organici

NemasuratiMgCa

NH4

MasuratiNaK

UAG (Gap-ul anionic urinar)GA=N

UAGN∼≥0 Inutila: cetoacidoza

+(NAE mica) -20-(-50) (NAE mare)

RTA tip I (distal)RTA tip II (proximal) (variabil)RTA tip IV (hipoaldosteronism

hiporeninemic)IRA (variabil)IRC (variabil)Acetazolamida (variabil)

NON RENALA

DiareeFistule pancreatice/intestNaCl 0,9%etc

Osmolii si gap-ul osmolar

Osmol: cant de subst (contine NA=6,023 x 1023 molecule/ml) dintr-o solutie ideala ce scade punctul de congelare al solventului pur cu K° (ptr apa K °=1,86)

Osmolalitate (A)-mosm / kg- Masurata in laborator

Osmolaritate (B)-mosm / l- valoare calculata

GAP=A-B (N∼0)

2 (Na) + (Glu mg/dl)/18 + (BUN mg/dl)/2,8

Osmolii si gap-ul osmolar

DK

Glicogenoliza

Ac. lactica

Lipoliza+ corpi cetonici

Metanol, Etilenglicol, Alte toxice

GAP crescut

Corpi cetonici

Alk. Ket.

Osmolii si gap-ul osmolar

Alc. isopropilic

HiperlipidemieManitol

GAP crescutPseudo hNa

Osmolaritate ↓GAP ↑aparent

Ig iv + maltoza

Alcaloza metabolica si Cl-ul urinar

Mentinerea alcalozei metabolice

The enemy of my enemy is my friend…

BOSTONHCO3/CO2

approach

COPENHAGABE/BD

approach

P

E

T

E

R

S

T

E

W

A

R

T

Peter A. Stewart

�Nascut in Winnipeg, Maniteba, Canada

�Ofiter in Fortele Marine Canadiene (WWII)

�MS in fizica si matematica (1949)

�PhD in biofizica (1951)

�Domenii de interes: neurofiziologie, fiziologie generala, biologie moleculara

�Matematica, fizica, chimia, biologia = unificate

�1981 – “How to understand acid-base physiology”

Ce determina pH-ul?

HCO3 (Na) OH- (Na) H+(Cl-)

Ce determina ph-ul?

• [H+] x [OH-] =kw

• [H+] +[Na+]= [Cl-] + [OH-]

• [H+] +[Na+] - [Cl-] - [OH-] =0

• [H+] – (kw/ [H+]) + SID = 0

• [H+]2 + SID x [H+] – kw = 0

• [H+]=Rad (kw + SID2/4) – (SID/2)

• [OH] = Rad (kw+ SID2/4) + (SID/2)

• [H+] x [OH] = kw + (SID2/4) - (SID2/4)=kw

H2O; kw=10-14; pH=7; t°=25°C+

NaOH HCl

Ce determina pH-ul?

Conservarea masei

Principiul isohidric (simultaneitatea echilibrelor de

disociere)

Principiul electroneutralitatii

1. Disocierea apei: [H+]+[OH-]=Kw x H2O

2. Disocierea ac slabi: [H+]+[A-]=Ka x [HA]

3. Conservarea masei a. slabi: [HA]+[A-]=[Atot]

4. Formarea HCO3: [H+]+[HCO3-]=K1 x PCO2

5. Formarea CO32-: [H+]+[CO3

2-]=K2 x [HCO3-]

6. Electroneutralitate: SID+[H+]-[HCO3-]- [A-]- [CO3

2-]-[OH-]= 0

SID(N)=40 – 44 mEq/l

-3 variabile independente-5 constante-variabile dependente: [H+],[OH-] ,[HA], [A-], [HCO3

-], [CO32-]

! (mmoles)

mEq�pH dep

Modelul STEWART - Dezavantaje

1. O valoare corecta pentru SID este greu de obtinut2. Valoarea pentru ATOT este pH dependenta cand este exprimata in mEq3. Un grup heterogen de acizi slabi (in principal albumina, fosfatii) este

privit ca un singur acid slab4. Valorile pentru ATOT si Ka sunt slab documentate

Prezice pH-ul ±0,05U

WATSON STEWART FIGGE

MulticompartimentalBicompartimental

Modelul Stewart este “orb”?

Ecuatia Henderson Hasselbach vs Stewart

- pk1’ aparent dependent de pH, concentratia proteinelor, concentratia Na- Relatia liniara log PCO2 – pH (pentru HCO3=const) este “muscata” de

conc. ∆ Prot, ∆ Na, ∆ Cl, pH acid

∆pH↓ (t=const, IS=const): SID, SCO2, Ka, ATOT = const

Tulburari AB primare

PaCO2 SID ATOT

Trei variabile independente

Tulburari AB primare

SIDA= 40 mEq/L (N)SIDB= 20 mEq/L(Na/Cl)A= (Na/Cl)B =NACIDOZA DE DILUTIEEx: manitol, hiperglicemie, etilenglicol, metanol � ↑ ECF

Na 140Cl 100

Na 70Cl 50

1L

+1L H2O

A B

Na 140Cl 100

Na 280Cl 200

2L

-1L H2O

A B

Na 70Cl 50

Na 86,8Cl 70,8

2L

+500ml SF

A B

Na 280Cl 200

Na 345,45Cl 181,8

1L

+100ml NaHCO3 8,4%

A B

SIDA= 40 mEq/L (N)SIDB= 80 mEq/L(Na/Cl)A= (Na/Cl)B =NALCALOZA DE CONTRACTIEEx: diuretice

SIDA= 20 mEq/L (Na/Cl=1,4=N)SIDSF ∼ 0 SIDB= 16 mEq/LClcor=Clobsv x Na norm/ Na obsvClcor=114ACIDOZA DE DILUTIE+ACIDOZA HIPERCLOREMICA

SIDA= 80 mEq/L (Na/Cl=1,4=N)SIDsol = 100 SIDB= 163,64 mEq/LClcor=73,67

ALCALOZA + ALCALOZA DE CONTRACTIE HIPOCLOREMICA

2,5L

1L

2L

1,1L

SIG – Strong Ion Gap (Stewart-Fencl)

Altii +

Ca2+ Mg2+

Na+

K+

Cl-

HCO3-

Pi-

Alb-

La-

Altii-SIDa=SI+-SI-=WI- -WI+

SIDa=(Na+K+Ca+Mg)-Cl-LaSIDe=Alb-+Pi-+HCO3-

SIDa-SIDe=SIG < 5-8 mEq/L (N)

HCO3- -- cel actualAlb-=Alb(0,123 x pH-0,631)

Pi-=Pi(0,309pH-0,469)Alb – g/L

Pi – mol/L

SIDa = Alb-+Pi-+HCO3-+Altii- -Altii+

SIG= Altii- -Altii+

Altii � sunt atat SI cat si WA

SIG vs AG

Factor (bias) AG SIG

L-Lactate Increased No effect

[Pi] increase Increased No effect

[Pi] decrease Decreased No effect

pH increase Increased No effect

pH decrease Decreased No effect

[Ca2+] and [Mg2+]

increaseDecreased No effect

[Ca2+] and [Mg2+]

decreaseIncreased No effect

[Alb] increase Increased No effect

[Alb] decrease Decreased No effect

SIG vs AG

Factor (bias) AG SIG

Other unmeasured strong anions (eg. Ketoacids, salicylate, D-lactate)

Increased Increased

Unmeasured weak anions (eg. Polygelinate, myeloma IgA band)

Increased Increased

Unmeasured strong cations (eg. Lithium) Decreased Decreased

Unmeasured weak cations (eg. THAMH+, myeloma IgG band)

Decreased Decreased

Chloride over-estimation (bromism, hyperlipidemia, high bicarbonate)

Decreased Decreased

Sodium under-estimation (severe hypernatremia)

Decreased Decreased

SIG vs AG (dependenta pH)

Trei lucruri despre SIG:

1. SIG trebuie corectat in functie de apa

SIGcor=SIGobsv x Nanormal/Naobservat

2. SIG este “orb” cand Altii+=Altii-

(Ex – cetoacizi (SIG↑) si hipernatremie severa (SIG↓))

3. Scoaterea Ca++, Mg++ din ecuatie(∼constante) poate ascunde pana la 4 mEq/L din Altii- (L-)

BE gap (Gilfix approach)BE=parametru sangvin, nu plasmatic

1. Daca ATOT≠N ⇒∆BB trebuie corectat pentru albumina si fosfat (Ex. Alb ↓)a. albumin effect (mEq/L)= (42 g/L – albumina g/L) x (0,123 x pH – 0,631)b. phosphate effect = (1 mmol/L- fosfat mol/L) x (0,309 pH – 0,469)

2. Daca ATOT=N ⇒∆BB=X=SIG poate fi corectat pentru:a. Water effect (mEq/L)

BE=SIG=∆SID=SIDobsv – SIDN

Sa pres. ca e doar “water effect” nu si X-

SIDobsv=Naobsv/140 x SIDcor

SIDcor = SIDN

b. Chloride effect (mEq/L)Clnorm – Cl cor = 102- Clobsv x Nanorm/Naobsv= 102-Cl obsv x 140/Na obsv

PUSH

BE gap

“Altii” = SBE- watter effect- Cl effect- Alb effect – P effect

“Altii” =SBE- Na/Cl effect – Alb effect

BE gap AG SIG

0,25 (42- Alb g/L)Na-Cl-38

SOFISM…

Stewart in 1983 reintroduced plasma buffer base under the name“strong ion difference”(SID). Buffer base was originally introduced bySinger and Hastings in 1948. Plasma buffer base, which is practically equalto the sum of bicarbonate and albuminate anions, may be increased due toan excess of base or due to an increased albumin concentration.

Singer and Hastings did not consider changes in albumin as acid-basedisorders and therefore used the base excess, i.e, the actual buffer baseminus the buffer base at normal pH and pCO2, as measure of a non-respiratory acid-base disturbance. Stewart and followers, however,consider changes in albumin concentration to be acid-base disturbances: apacient with normal pH, pCO2, and base excess but with increased plasmabuffer base due to increased plasma albumin concentration get thediagnoses metabolic (strong ion) alkalosis (because plasma buffer base isincreased) combined with metabolic hyperalbuminaemic acidosis.

Extrapolating to hole blood, anemia and polycytaemia shouldrepresent types of metabolic alkalosis and acidosis. This reveals that theStewart approach is absurd and anachronistic.

Acta Anaesthesiol Suppl, 1995; 107:123-8 – Sigaard-Andersen O, Fogh-Andersen N.