Acid Base Physiology – Stewart and beyond
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Transcript of Acid Base Physiology – Stewart and beyond
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Notiuni fundamentale in EAB
SUUB
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EAB
1. Notiuni fundamentale
2. Factori etiologici
-- mecanisme fiziopatologice
-- diagnostic diferential si pozitiv
-- tratament specific
3. Tratament general (nespecific)
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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
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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
-)
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pH-ul neutru
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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
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EC pH este un surogat pentru IC pH
Spatiul extracelular
Ox
OzOy
CzCy
Cx
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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-
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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
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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
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Totul este relativ ……
Buffer eficient ⇒ pKa ε [pH-1,5 ; pH+1,5]
pK5,9
pK8,9
Buffer ionsStrong ions Strong ions
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Totul e relativ…
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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
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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
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Raspunsul mecanismelor compensatorii in ACM si ALM
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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
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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
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Sistem tampon (inchis)
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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
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Sisteme tampon sanguine HCO3/CO2
inchis vs deschis
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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
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Ecuatia Henderson - Hasselbach
Buffer slab aparent
K1 K2 K3
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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)
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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
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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
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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
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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
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Diagramele Davenport
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Diagrame Davenport
METABOLIC ALKALOSIS
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Diagrame Davenport
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Diagrame Davenport
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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
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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
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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→)
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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
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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?
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BOSTON
WINTERS
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BOSTON
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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
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COPENHAGA
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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
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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
+
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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
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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
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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
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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+
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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
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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
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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
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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
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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
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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
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Osmolii si gap-ul osmolar
DK
Glicogenoliza
Ac. lactica
Lipoliza+ corpi cetonici
Metanol, Etilenglicol, Alte toxice
GAP crescut
Corpi cetonici
Alk. Ket.
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Osmolii si gap-ul osmolar
Alc. isopropilic
HiperlipidemieManitol
GAP crescutPseudo hNa
Osmolaritate ↓GAP ↑aparent
Ig iv + maltoza
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Alcaloza metabolica si Cl-ul urinar
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Mentinerea alcalozei metabolice
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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
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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”
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Ce determina pH-ul?
HCO3 (Na) OH- (Na) H+(Cl-)
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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
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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
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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
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Modelul Stewart este “orb”?
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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
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Tulburari AB primare
PaCO2 SID ATOT
Trei variabile independente
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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
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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
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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
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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
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SIG vs AG (dependenta pH)
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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-)
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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
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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
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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.