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History, Resp. D, CLD, CKD, conscious level, recurrent renal stones, DM, Volume Status, BP,
ventilation, electrolytes, Urine Analysis, Plasma Osmolality, Plasma Osmolality Gap, Drugs
(insulin, biguanids, diuretics, NA HCO3 usage, alcohol, licorice, salicylate, ethanol, methanol,..
etc.), (Urology & GUT surgeries) ECG, s.CREAT, s.K, s.CL, s.ALBUMIN, s.CA, s.LACTIC ACID, etc.
Asses the VALIDITY: - H
+
=
(Pco2/HCO3)*24 = (7.8-
PH)*100.
Asses is it Arterial or Venous sample: - check
Pco2, Po2 and SatO2. Central venous pH is 0.03-
0.05 ABG & Pco2 4-5mmHg ABG.

Identify the Primary Disturbance
Arterial
PH 7.4
Acidosis
PH = 7.4
with abnormal Pco2, HCO3
Mixed acid base
PH 7.4
Alkalosis
Look at Pco2, HCO3: - (both move in the
same direction except in mixed disorders)
Reapete ABG

N.B.: causes of LOW SERUM ANION GAP ( 7 mmol/l): -
1.Most common cause is laboratory error.
2.Hypoalbuminemia.
3.A rise in unmeasured cations (hyperkalemia,
hypercalcemia, hypermagnesaemia, or severe
lithium intoxication).
4.The serum chloride concentration is
overestimated (pseudohyperchloremia)[
Marked hyperlipidemia, Bromide ingestion].
5.If none of these disorders is present, a serum
protein electrophoresis should be obtained
to look for a cationic Para protein that is
present in some patients with multiple
myeloma.

PH PaCO2 HCO
3
-

Resp. acidosis
Resp. alkalosis
Meta. acidosis
Meta. alkalosis

1.In a simple acid-base disorder, the secondary response never
fully corrects the ph. They bring pH back toward normal.
If they fully correct the pH or overshoot, it is a mixed acid-
base disorder.
2.In a simple acid-base disorder, the appropriate secondary
response must be present. If they are not present, it is a
mixed disorder.
3.In a simple acid-base disturbance the plasma bicarbonate and CO2
concentrations change in the same direction. If they don't, it is a
mixed disorder.
4.Note that any combination is possible, except concurrent
respiratory acidosis and respiratory alkalosis, since a
person cannot breathe too fast and too slow at the same
time.




































If Pco2 is the initial or main chemical change, then
process is Respiratory. (Normal Pco2=40 mmHg).
If HCO3 is the initial or main chemical change, then
process is Metabolic. (Normal HCO3=24 mmHg).
Asses the Compensatory Response: (also asses
for Mixed disorders)

Asses the Compensatory Response: (also asses
for Mixed disorders)

Respiratory Acidosis Pco2 40 mmHg
Respiratory Alkalosis Pco240 mmHg
Acute HCO3 by 1
mmol/l for every 10
mmHg in Pco2 40
mmHg.
Chronic [12-24 hrs to
start2-3 days for full]
HCO3 by 4 mmol/l for
every 10 mmHg in
Pco2 40 mmHg.

Acute HCO3 by 2
mmol/l for every 10
mmHg in Pco2 40
mmHg.
Chronic [12-24 hrs to
start2-3 days for full]
HCO3 by 5 mmol/l for
every 10 mmHg in Pco2
40 mmHg.

Metabolic Alkalosis (HCO3 24 mmHg): - Expected Pco2=
(0.7*HCO3) + 20 range (+/-5). But compensation never make
Pco2 55 mmHg. URINARY [CL

] can help in differentiating.


Metabolic Acidosis(HCO3 24 mmHg): -
Expected Pco2= (1.5*HCO3) + 8 range (+/-2).

Calculating Anion Gap = [NA+] (CL- + HCO3-)
Normal Value = (12 4 meq/l).
High Anion Gap

in cases of hypoalbunemia: Corrected Anion
Gap = Anion Gap + [(4- s. albumin) * 2.5]
Normal Anion Gap
Calculate delta anion gap/HCO3 ratio
increase in serum AG 12
decrease in serum HCO3 24
To detect the associated hidden metabolic abnormality.
If 1 : -
If between 1 - 2 : -
If 2 : -
1. With urinary anion losses, as in some of
ketoacidosis, D-lactic acidosis, or toluene (if
late) intoxication.
2. In a combined high and normal AG acidosis,
as might occur if diarrhea were superimposed
upon any high AG metabolic acidosis or if
severe diarrhea led to reduced tissue
perfusion and lactic acidosis.
3. In some cases of chronic kidney disease.
High AG metabolic acidosis
concurrent with metabolic
alkalosis, as in vomiting with DKA,
or to the compensatory increase
in serum HCO3 induced by
preexisting chronic respiratory
acidosis (COPD).
Calculate the Urinary Anion Gap
Urine AG = Urine (Na + K - Cl)
To detect unmeasured NH4
If Negative value means
GIT loss.
(normal NH4 excretion)
If Positive value means
Urinary loss.

1. Diarrhea or other
intestinal losses (eg,
tube drainage).
2. Ureteral diversion
(due to Cl

/HCO3

exchange
in the bowel loop mucous
membrane).
1. Type 4 RTA
(hypoaldoste
ronism)
especially in
DM
nephropathy
.
2. Some cases
of chronic
kidney
disease.

Saline (chloride) sensitive
Effective ECV Contraction,
Normotension, K
+
Deficiency, and
Secondary Hyperreninemic
Hyperaldosteronism
That responds to chloride
administration (Nacl/KCl).
1. Common.
2. Urinary chloride >10mmol
Diuretic.
3. Urinary chloride
<10mmol GIT loss as in
villous adenoma and
vomiting.
4. . Post hypercapnia.

Chest: - Asthma, COPD, Sarcoidosis (IPF).
Central: - Benzodiazepines.
Muscles: - Guillain Barre, myasthenia gravis .

Anxiety, fever, psychogenic.
Pregnancy, Liver disease.
CNS causes: stroke, subarachnoid haemorrhage,
meningitis.
Drug use: doxapram, aspirin, caffeine and coffee
.abuse.
Pneumonia, Pulmonary Embolism.
: validity, (arterial or venous), (acidosis or alkalosis), (respiratory or metabolic),
(simple or mixed), compensated (acute or chronic if respiratory), corrected anion gap if metabolic (high AG or normal AG),
Delta ratio (if high AG {mixed with normal AG , met. alkalosis or pure high AG}), urinary AG (IN a normal AG metabolic acidosis).

Saline (chloride) resistant ECV
Expansion, Hypertension, K
+
Deficiency,
and Hypermineralocorticoidism
Not respond to chloride
administration (Nacl/KCl).
Less common.
Bartters, Gittlemans , Mg
depletion.
If Renin, aldosterone Both
high:
1. RAS
2. Renin secreting tumor
3. Malig HTN.
If Both low :
1. Cushings syndrome.
2. Exogenous
mineralocorticoids
excess.
3. Licorice.
4. Liddle syndrome.
Low renin high aldosterone:
1ry hyperaldosteronism.
If serumK3.5:

If serumK5.5:

Others:
1. Post treatment of ketoacidosis.
2. Carbonic anhydrase inhibitors.

1. Type 2 (proximal)
renal tubular
acidosis (RTA).
(urine pH < 5.5,
hypophosphatemia.)
2. Type 1 (distal)
RTA.
(urine pH > 5.5,
calcium phosphate
stones and
nephrocalcinosis.)
An uncomplicated high AG metabolic
1. Chronic renal failure.
2. Lactic acidosis. (Type A, type B, D-
lactic).
3. Ketoacidosis (Diabetes mellitus,
Starvation, Alcohol).
4. Ingestions:
o Methanol (P. osmolality gap).
o Ethylene glycol (P. osmolality gap,
oxalate crystals in urine).
o Aspirin (normal osmolality, mixed
respiratory alkalosis & metabolic
acidosis).
5. Toluene (if early).
6. Pyroglutamic acid (5-oxoproline).

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