In the name of ALLAH

ABG by Dr Saleh
Normal value
PH
7.4
- > 7.4 = alk
- < 7.4 = acidosis
PCO2
40
- > 40 = acidosis
- < 40 = alk

Normal value
HCO3
24
- > 24 = alk
- < 24 = acidosis
Anion gap 8-12 +/- 2 with K
10 +/- 2 without K
- > 12 = high anion gap
MA
- < 8 low AG
Equation
- Na [HCO3 + CL]
PO2
60
Osmolarity 285 310
hydrogen ion concentration increases by approximately 5.5 nmol/l for each
increase in pCO2 by 1 kPa in an acute disturbance
Equations
- anion gap : Na [Cl +HCO3]
- expected PCO2 in M Acidosis = 1.5 x HCO3 + 8 = the answer +/- 2
- Expected PCO2 in M Alk : 0.7 x HCO3 + 21 +/- 2
- delta delta to find third component for the acid base disturbance
o delta anion gap / delta HCO3
o If delta delta
> 1 = there is third metabolic alk [normal anion gap met acidosis or
anion gap met acidosis or metab alk]
= 1 = no addition component
< 1 = non anion gap metabolic acidosis
To know the 1ry of PH disturbance use ROME
- resp opposite
- metabolic equal
PH 7.20 PCO2 30
HCO3 12
- Metabolic acidosis

Na 120

Cl 120

- Anion gap 120 [12 + 122 ] = 14 high anion gap MA

- In metabolic acidosis the body try to compensate by the PCO2
o Expected PCO2 : 1.5 x HCO2 + 8 = +/-2
12 x 1.5 = 18
18 + 8 = 26
The range of PCO2 if there is compensation should be from 24 28
The PCO2 30 more than the expected mean there is also R
Acidosis
- Dx : Normal anion gap metabolic acidosis + resp acidosis
- To find Third component for the PH disturbance we do what called delta
delta = Delta anion gap / delta HCO3
o Delta AG = 12 normal 14 = 2
o Delta HCO3 = 24 normal 12 = 12
o 2/12 = 0.16
o 0.25 < 1 this mean = non anion gap metabolic acidosis
What r the condition where u find High anion gap metabolic acidosis + resp
acidoses + normal/non anion gap metabolic acidosis
- Causes High anion gap metabolic acidosis : KUSSMAL
o K : Ketoacidosis
U : uremia
o S : salicylate poisoning
o S : sepsis
o M: Methanol + ethanol isopropyl ethylic glycol
How to diff ??? u need to send to the toxicology lab blood and urin
sample
Ethanol methanol
Isopropyl alcohol
o Will not cause high AG MA
o Only cause Inc the osmolar gap
ethylic glycol
o urin analysis shows Ca oxalate crystals seen in the
Microscopes has envelop shape can cause renal failure this
lead to high anion gap acidosis

o High osmolar gap : if the gap b/w the lab result and ur
calculation subtract the calculated from the measured is >
10 there is solute not known
o A : alcohol toxicity [ comatose with high AG MA + resp acidosis due
to inh of the resp center normal aG MA]
o L : lactic acidosis
- Normal anion gap metabolic acidosis
o Renal tubular acidosis [RTA]
Type 1 2 4
All hypoK except 4 hyperK
High urin anion gap in urin in type 1
Most common cause of type 4 : Diabetes
o GI loss

RTA
Hyperchloremic acidosis with a normal anion gap and normal (or near
normal) GFR, and in the absence of diarrhea, defines RTA
Type 1 [ distal
Type II [ proximal Type VI
tubular ]
tubule ]
[Hyporeninemic
hypoaldosteronemic]
Causes - Congenital
- Congenital, e.g. Type IV is the
- Hyperglobulinae
Fanconi's
most common RTA in
{2}
mia
syndrome ,
clinical practice
- Autoimmune
cystinosis,
- Diabetes
connective tissue
Wilson's disease
nephropathy
diseases, e.g. SLE - Paraproteinaemi - Tubulointerstitial
- Sjgren
a, e.g. multiple
renal dis
syndrome
myeloma
- HTN

- Toxins and drugs, - Amyloidosis

nephrosclerosis
e.g. toluene,
- Hyperparathyroi - AIDS
lithium,
dism
- Hypoaldosteronism
amphotericin
- Heavy metal
(1ry or secondary)
toxicity, e.g. Pb, - Obstructive
Cd, Hg
nephropathy
- Drugs, e.g.
- Drugs, e.g.
amiloride,
carbonic
spironolactone,
anhydrase
triamterene. TMP,
inhibitors
pentamidine
acetazolamide - Renal transplant
, ifosfamide
rejection
Mechani Decreased hydrogen proximal HCO3
sm
ion (acid) excretion reabsorption =
into the urine
bicarbonaturia
distal
acidification
Acidosis sever
Urine
>5.3 = alk urin
pH
during
acidemia
Urin
Anion
gap

+
EXP :urinary
excretion of
NH4+Cl is
decreased, and the
urinary anion gap is
positive

Moderate
Variable: Usually
at the steady state
urin PH < 5.3 =
acidic, but can be
initially alk
high . [1]
+/-

Aldosterone deficiency
/Resistance/antagonis
m. Causing Distal Na+
reabsorption, K+
secretion, and H+
secretion
Mild
Usually < 5.3

Titratabl titratable acid

e acid
excretion
EXP : alk urin inh H
binding to HPO4-2
Plasma Very low (may be <
HCO3-, 10 mEq/L).
untreate
d
Fe
<3%
HCO3
Plasma or normal.
K+
EXP :
- Enhanced K+
excretion occurs
probably because
there is less
competition from
H+ in the distal
nephron transport
system
- hyperaldosteronis
m occurs in
response to renal
salt wasting,
which will K
excretion
clinical - Hyperchloremic
presenta
Metabolic
tion
acidosis
- CL + HCO3 =
non AG MA
- hypercalcinuria
Nonelec - Nephrocalcinosis
trolytic - Recurrent Ca

Normal

Moderately low
(14--20 mEq/L).

Usually > 15 mEq/L

> 15%

< 3%

or normal.
High K
EXP
The delivery of
HCO3 to the distal
nephron K+
secretion, and
hypok results if a
patient is loaded
with excess HCO3
without adequately
supplemented of K.

- Hyperchloremic
Metabolic
acidosis
- Urinary K
wasting
hypoK
- Rickets or
None
osteomalacia

complic
ations

ttt

kidney stones.=
nephrolithiasis
chronic acidosis
dec tubular calcium
reabsorption
Hypercalciuria,
alkaline urine, and
lowered level of
urinary citrate cause
calcium phosphate
stones and
nephrocalcinosis
NaHCO3 (13
NaHCO3 or
mEq/kg/d)
KHCO3 (1015
mEq/kg/d),
thiazide

Fludrocortisone (0.1
0.5 mg/d),
dietary K+ restriction

furosemide (40160
Treat associated
mg/d),
diseases and
institute Na+
NaHCO3 (13 mEq/
restriction bec
kg/d)
Hypok worsened
Na+ restriction
with exogenous
sodium bicarbonate
[1]
About 90% of filtered HCO3 is absorbed by the proximal tubule. A
proximal defect in HCO3 reabsorption will overwhelm the distal tubules
limited capacity to reabsorb HCO3, resulting in bicarbonaturia [alk urin]
and metabolic acidosis. Distal delivery of HCO3 declines as the plasma
HCO3 level decreases. When the plasma HCO3 level drops to 1518 mEq/L,
the distal nephron can reabsorb the diminished filtered load of HCO3
Bicarbonaturia resolves, and the urinary pH can be acidic [acid urin]
{2}
Any of the proximal type 2 RTA etiologies can lead to Fanconi's syndrome,
reflecting generalized proximal tubule dysfunction. Think Fanconi's
syndrome if you see hypophosphatemia, hyperuricosuria, and glycosuria
despite normal serum glucose levels.

Metabolic alk :
- Eg : PH 7.5 HCO3 30
PCO2 50
o M alk
o The PCO2 should inc as a compensation
Expected PCO2 : 0.7 x HCO3 + 21 = +/- 2
42 = the range 40 - 44
PCO2 higher than the expected this mean there is also resp
acidosis
- NOTE if the pt PCO2 is with the range of expected PCO2 then there
will be no resp acidosis but it will never called compensated except if the
PH return to normal
Respiratory disturbances
PH
Resp acidosis

Resp alk

Acute
0.08 x delta PCO2 over 10
HCO3 Compensation for each
10 CO2 inc from normal 40
the HCO3 should inc by 1
above 24 normal biocarb
HCO3 should dec by 2

Chronic
O.03 x delta PCO2 /10
HCO3 should inc by
3.5
HCO3 should dec by
5

What is the AA gradient in resp acidosis or alk

- normal AA gradient mean the pt has drug overdose
- bec all the other causes [PE, pneumonia, pulm edema, ARDS] of resp
acidosis r associated with high AA gradient except drug overdose with
normal AA gradient
Eg PH 7.23
PCO2 60
HCO3 35
- with this high retained PCO2 + high HCO3 u should expect chronic
lung dis like COPD with exacerbation infection
- the PCO2 above normal by 20 so we should add 2 to the normal
HCO3
o expected HCO3 24 + 2 = 26

o as the pt has higher HCO3 than expected this mean he is suffering

also from Metabolic alk
- when u have resp acidosis and Metabolic alk u should look for K in 90
% of the cases u find the pt with hypoK if the K corrected the HCO3
will gradually dec
- NOTE : in COPD pt the Neb dec the K more
What r the causes of acute resp alk
- salicylate cause high anion gap Metab acidosis and resp alk
- central cause which cause hypopnea or apnea any think affect the resp
center
o Eg in ICH
o Or any cause of brain edema
- Pulm embolism
How to know it is acute or chronic without Hx
- Acute PH = 0.08 x delta PCO2 over 10
- Chronic PH = O.03 x delta PCO2 over 10
Eg PH 7.55
PCO2 20
HCO3 22
- resp alk
- to know if it is acute or chronic
o PH = 0.08 x delta PCO2 / 10
o Delta PCO2 = 40 20 = 20
o 20 x 0.08 = 0.6
o 1.6 / 10 = 0.16
o PH is expected to inc in alk thus we add 0.16 to the normal PH 7.4
0.16 + 7.4 digits after the normal PH = 7.56 it is near the PH
of the pt
o This indicate that this PH is of the acute resp alk
- the PCO2 less than the normal by 20 thus we should subtract from
normal HCO3 4
o 24 4 = 20

o The HCO is higher than the expected this mean there is also
metabolic alk
Examples
- case 24 yo female found comatose on the floor. On arrival O2 sat 88 pin
pointed pupil PH 7.25 PCO2 60
PO2 65
HCO3 26
o causes of pin-pointed pupil
Intra-pontain Hrge
Cocaine heroine
Organo-phosphorous
Ptosis and myosis in Horner syndrome
o Resp acidosis
o Compensation for resp acidosis depend is it acute or chronic from
the Hx it seems to be acute
o To know is it acute or chronic
0.08 x delta PCO2 / 10
0.08 x 20 / 10 = 0.16
Normal PH the 0.16 bec in acidosis the PH is expected to dec
7.40 0.16 = 7.24 it is near to the no. we have 7.26
This mean the case is acute resp acidosis
o Expected HCO3
For each inc in PCO2 we add 1 to the normal biocarb bec as
compensation for the acidosis we expect to have metab alk
24 +2 26
The same value as the biocarb we have
This called acute resp acidosis only bec the biocarb the pt has is
the same as the expected biocarb. We dont called it compensated
metab alk bec the PH is not normal
o The AA gradient normal
o This pt found to have heroine overdose
The cause of pinpoint pupil
The cause of resp suppression and resp acidosis
- 60 yo man Dx ALS amyotrophic lateral sclerosis, presented with dec
LOC. PH 7.37
PCO2 57
PO2 70 HCO3 32

o Resp acidosis
o Why pt with ALS come with dec LOC as the dis progress the pt
develop resp depression with recurrent pneumonia and become
ventilator depended eventually
o To know is it acute or chronic
PH in acute = 0.08 x delta PCO2 / 10 = 0.13
Normal PH 7.40 0.13 = 7.27
PH in chronic = 0.03 x delta PCO2 / 10 = 0.05
Normal PH 7.40 0.05 = 7.35
o The expected HCO3 in chronic resp acidosis
For each 10 inc in PCO2 should inc the HCO3 by 3.5
24 + 7 = 31
o The dx resp acidosis compensated by metabolic alk bec the HCO3 is
in the expected range and the PH is in the normal range
- 55 yo male pt k/c of congestive HF presented with acute SOB. pt DM and
has cough with sputum PH 7.22 HCO14 PCO2 55 Na 130 Cl 100
o Metabolic acidosis
10/24 x 100 = 41 % metabolic acidosis
15/40 x 100 = 37 %
o Expected PCO2 in metabolic acidosis =
1.5 x HCO3 + 8 +/-2 = 29. The range 31- 27
PCO2 55 away from the range this mean there is also Resp
acidosis = Dx 1ry metabolic alk with resp acidosis. Possible
causes for resp acidosis in this case
Acute SOB
Pneumonia
Pulm edema : alv full of excretion with less exchange of O2
o Anion gap = 130 114 = 16 high anion gap met acidosis. The cause
in this pt could be : Infection sepsis
o Delta delta
Delta anion gap / delta HCO3 = 4/10 = 0.4
0.4 < than 1 non anion gap met acidosis
The cause could be RTA type 4 specially if the K is high

 GI loss [diarrhea]
If we assume that delta-delta is > 1 the third component could be
met alk. What could be the cause in this pt
Due to diuretics over dose
Vomiting/diarrhea causing hypoK
o Dx : Metabolic acidosis e resp acidosis non ion gap met acidosis
- 60 yo smacker taking 2 neb. Not able to talk. PH7.29 PCO2 65 PO2 55
HCO3 30
o Resp Acidosis
o To know acute of chronic resp acidosis
PH in Acute resp = 0.08 x delta PCO2 / 10 = 0.2
In acidosis we subtract the result from the normal PH : PH
7.40 0.2 = 7.2
In chronic PH = 0.03 x delta PCO2 / 10 = 0.07
PH = 7.40 7.07 = 7.33
More near to our PH this mean we have chronic res acidosis
o The expected HCO3 as a compensation is 3.5 for each inc in PCO2
PCO2 2.5 more than the normal
The HCO3 should inc 2.5 x 3.5 = 8
24 + 8 = 32
Expected HCO3 is less than the HCO3 of the pt
This mean we have also metabolic acidosis
PH 7.40 HCO3 24
CO2 40
Na 145
Cl 90
- Is it normal ABG : NOOOOO first u should chick the anion gap
- anion gap : 31 high anion gap = abnormal ABG
- Delta delta : 19 / 0 = 0
was Q in their exam and no one now the answer
- Serum osmolarity 350 PH 7.30 HCO3 12
CL 100
Glu 250
o metabolic acidosis

PCO2 25

Na 130

o anion gap = 18 high anion gap metabolic acidosis

o expected PCO2 = 1.5 x delta HCO3 + 8 = 26
range 24 - 28
PCO2 within the range no resp disturbances
o Delta delta 6/ 12 = 0.5 < 1 mean non AG Metabolic acidosis
o Serum osmolarity
2 x Na + glu/18 + bun /2.8 = 13.8 + 5 + 260 = 278
There is high osmolar gap b/w the measured and calculated
Could be due to ethylene glycol chara by present of Ca
oxalate crystals in urin + Renal Failure
Methanol
Ethanol
Isopropanol : is not a cause her bec it only cause high osmolar
gap no metabolic acidosis
o If this pt was comatose on presentation: give thiamin vit B12