Acid Base Disorders
Prof. Tahir Shafi
Why should we know about acid base
disorders
 What are acid base disorders
 How to interpret acid base disorder
 How to establish the cause

Why to worry about acid base
disorders
Acid base homeostasis fundamental for
maintaining life
 Extreme acidemia or alkalemia can

◦ alter tertiary protein structure affecting
enzyme activities ion transport
◦ alter almost every metabolic pathway

Extreme acidemia can
◦ depress cardiac function, impair the vascular
response to catecholamines, and cause
arteriolar vasodilation and venoconstriction,
with resultant systemic hypotension and
pulmonary edema.

Alkalemia can cause
◦ cardiac arrhythmias, neuromuscular
irritability, and contribute to tissue hypoxemia.
◦ fall in cerebral and myocardial blood flow
◦ respiratory depression
◦ potassium abnormalities a common
accompaniment of acid-base disorders, also
contribute to the morbidity.

Identification of mild to moderate
disorders can give you important clue to
the presence of unsuspected but may be
otherwise important medical conditions
A patient has the following lab tests:
ABG pH
7.4
PO2
100 mmHg
PCO2
40
Bicarb
24 meq/l
Sodium
140
Potassium
4,2
Chloride
80
Bicarb
24
Creatinine 0.9
Glucose
110
 Which one of the following statements is correct
A. He has normal acid base parameters
B. He has metabolic acidosis and respiratory alkalosis
C. He has metabolic alkalosis and respiratory acidosis
D. He has metabolic acidosis and metabolic alkalosis
Regulation of acid base status
Acidity in the ECF measured by [H]+
 H+ = 38-42 nEq/L
 Average = 0.00004 mEq/L = 40 nEq/L
 pH - negative log of H+ in moles
 Maintenance of arterial pH within normal
range 7.38-7.42 with average pH 7.4

Henderson Hasselbach equation
Base
pH = pk + log
Acid
6.1 + log
HCO3
24
24
H2CO3
apCO2
1.2
a =0.03
Log 20
1.3 =7.4
Kassirer - Bleich Equation
H+ = 24 x
pCO2
HCO3
pH and H+ are inversely related
 h H+ results in i pH - Acidemia
 i H+ and hpH – Alkalemia
 Normal pH or H+ - Euphemia

Types of acid base disorders
Acidosis
pCO2
Respiratory
Alkalosis
H+ = 24 x
HCO3
Metabolic
Alkalosis
Acidosis
Stabilization of H+ for every primary disorder
there must be physiological compensation by
the opposite system
Compensations are predictable and can calculated
Respiratory compensation
H+ = 24 x
Primary
pH Initial
event
Met.
Acidosis
i
Met.
Alkalosis
h
pCO2
HCO3
Comp
Resp
Expected Cpmpensation
iHCO3
ipCO2
For 1 meq iHCO3, pCO2 i by 1-1.3 mmHg
PCO2 = HCO3+ 15
PCO2 = last 2 digits of pH
pCO2 = (HCO3) x 1.5+8+2 Winter’s
equation
hHCO3
hpCO2
For 1 meq h HCO3,PCO2 h by 0.6 mmHg
PCO2 =(HCO3 x 0.9) + 9
PCO2 =(HCO3 x 0.7) + 20
Metabolic compensation
H+ = 24 x
pCO2
HCO3
Primary
pH
Initial
event
Comp
Resp
Expected Cpmpensation
Ac. Resp.
Acidosis
i
hpCO
hHCO3
For every 10 mmHg h PCO2 ,HCO3 h by 1
Ch. Resp.
Acidosis
i
hPCO
hHCO3
For every 10 mmHg h PCO2, HCO3 h by 3.5
Acute Resp
Alkalosis
h
ipCO
iHCO3
For every 10 mmHg i PCO2, HCO3 i by 2
Ch. Resp
Alkalosis
h
ipCO2
iHCO3
For every 10 mmHg i PCO2, HCO3 i by 5
Rates of correction
Buffers function almost instantaneously
 Respiratory mechanisms take several
minutes to hours
 Renal mechanisms may take several hours
to days

15
Classification acid base disorders

Simple
◦
◦
◦
◦
Metabolic acidosis
Metabolic alkalosis
Respiratory acidosis
Respiratory alkalosis
 Primary change in one component
 Secondary change in the other component within physiological range
 Change in ph in the direction of primary change

Mixed
◦ Double
 Primary change with incomplete or over compensation with other
component
◦ Triple
◦ Quadruple
Normal acid base homeostasis
Metabolic acidosis
Exogenous
load
HCl
Other acids
Types of metabolic acidosis

Addition of acid other than HCl
◦ Serum chloride normal, bicarbonate low
◦ High anion metabolic acidosis

Addition of HCl
◦ Serum chloride high, bicarbonate low
◦ Normal anion or hyperchloremic metabolic
acidosis
Anion gap
Albumin is a major source of unmeasured
anions!
 Corrected AG = Observed AG + 2.5 x
(4.5 – measured albumin)
 If serum albumin is high, corrected anion
gap will be lower

Metabolic Acidosis
Causes of high Anion Gap metabolic acidosis
K
Diabetic Ketoacidosis
U
S
S
M
A
U
L
Uremia
Salicylate intoxication
Starvation ketosis
Methanol ingestion
Alcohol ketoacidosis
Unmeasured Osmoles, Ethylene Glycol, Paraldehyde
Lactic acidosis
MUDPILES Methanol, Uremia, DKA, Paraldehyde, INH/Iron
toxicity, Lactic acidodis, Ethanol/Ethlene glycol,
Salicylate toxicity
Metabolic Acidosis
Causes of normal Anion Gap metabolic
acidosis
H
A
R
D
U
P
Hyperalimentation
Acetazolamide
Renal tubular acidosis
Diarrhoea
Uretero sigmoidostomy
Pancreatic fistula
D – Diarrhea
 U – Ureteral diversion
 R – Renal tubular acidosis
 H – Hyperalimentation
 A – Acetazolamide
 M - Miscellaneous (toluene, amphotericin B

Hyperchloremic metabolic acidosis
Normal or high ammonia excretion
 Decreased ammonia excretion

Urine anion gap
Negative urine anion gap
positive urine anion gap
Urine osmolal gap


Measured urine osmolality – calculated urine
osmolality
Calculated urine osmolality
= 2 (UNa + UK )+ Urea
6
< 150 mosm /l= impaired NH4 excretion
>150 mosm/l = increased NH4 excretion
Urine ammonia level = half urine osmolal gap
Metabolic acidosis & osmolal gap

Ethyl Alcohol
Acetaldehyde
Acetic Acid

Methyl Alcohol

Ethylene Alcohol
Glycoaldehyde
Glycooxalic acid
Oxalic acid

OSMOLAL GAP = Measured osmolality- calculated
osmolality
Normal = < 10-15 mOsmol/Kg of H2O
Formaldhyde
Formic Acid
Glycolic acid
Urea
BS
Calculated serum osmolaliy = 2(Na) + 6 + 18
Metabolic alkalosis
Addition of base or loss of acid from
body
 High pH, high bicarbonate, high pCO2

Metabolic alkalosis
Saline responsive alkalosis
Saline resistant alkalosis
Low urinary Cl- (<10 mmol/l)
High Urinary Cl- (>10 mmol/l)
Normal or low BP
Normal BP
vomiting
Post diuretics
After hypercapnia
K+ depletion
Refeeding alkalosis
Bartter’s syndrome
Diuretics
Mg++ depletion
Severe K+ depletion
High BP
Reno vascular
disease
Conn’s syndrome
Cushing’s syndrome
More then one problem?
The “gap-gap” or “delta-delta” ratio
 In the presence of a high AG metabolic
acidosis, ? another metabolic acid base
disorder
 Comparing the AG excess to the HCO3
deficit - D AG =D HCO3
 D AG = (Observed AG – 12)
 D HCO3 = (Observed – Normal HCO3)

Mixed metabolic acid base
disorders
Coexistent
Metabolic alkalosis
delta/delta > 1 hh D AG
D HCO3
hh
Coexistent
Hypercholemic acidosis
delta/ delta <1
Mixed metabolic acid base
disorders
Corrected bicarbonate = observed
biacrbonate + D AG
 > 24 meq/l g Metabolic Alkalosis
 < 24 meq/l g Metabolic Acidosis

Respiratory acid base disorders
Respiratory acidosis
Hypoventilation
H+ = 24 x
Respiratory alkalosis
Hyperventilation
pCO2
HCO3
Primary event
Change in pCO2
Respiratory Alkalosis or Acidosis

Neuro respiratory control
◦ Central hypo or hyperventilation
◦ Intrinsic lung disease
A-a gradient (Alveolar arterial gradient)
Alveolar O2 =(760 – 47) * 0.21* PCO2/0.8
=100

Atmospheric pressure – water vapor pressure * FiO2* PaCO2
Arterial (a) =100
A-a gradient normal is < 10 in adults and
< 20 in elderly
Respiratory Alkalosis

Low pCO2, low bicarbonate, high pH
◦ A–a difference >10 mm Hg (>20 mm Hg in
elderly) - Hyperventilation with intrinsic lung
disease, ventilation–perfusion mismatch, or
both (e.g., pneumonia, pulmonary embolism)
◦ A–a difference <10 mm Hg (<20 mm Hg in
elderly) Hyperventilation without intrinsic
lung disease (e.g., fever, pregnancy)
Respiratory Acidosis

High pCO2, high bicarbonate, low pH
◦ A–a difference >10 mm Hg (>20 mm Hg in
elderly) Hypoventilation with intrinsic lung
disease, ventilation–perfusion mismatch, or
both (e.g., pneumonia, pulmonary embolism)
◦ A–a difference <10 mm Hg (<20 mm Hg in
elderly) - Hypoventilation without intrinsic
lung disease (CNS suppression)
Approach to Acid Base
Disorders
History
 Physical examination
 Serum electrolytes

◦ Anion gap
◦ Delta/delta ratio
Arterial blood gases
 Urinary electrolytes – Urinary anion gap
urine osmolal gap
 Serum osmolal gap

Acid Base Analysis
Step 1 : Look at pH. acidemic or alkalemic?
Step 2 : Look at pCO2
High – respiratory acidosis
Low – respiratory alkalosis
Step 3: Look at HCO3
High – metabolic alkalosis
Low – metabolic acidosis
Step 4: Determine primary event direction of pH
Step 5: Is it simple or mixed disorder.
compensatory response within
physiological range ?
Golden rules: 1- Mixed problem present if
only one component abnormal
2- Normal pH – both components
abnormal
3-Both components in same direction
Step 6 : Look at base excess if available
Step 7: If the respiratory disturbance is
present, is it acute or chronic?
Step 8 : Is there increased anion gap?
Step 9 : If anion gap increased, calculate
corrected HCO3 or delta/delta
Step 10 : Calculate osmolal gap if ingestion
of alcohols suspected
Step 11: Calculate urine anion gap or
osmolol gap
Acid Base Disorders
pH
PCO2
HCO3
Na+
ClK+
7.54
30 mmHg
25 meq/l
140 meq/l
92 meq/l
3.6 meq/l
Acid Base Disorders
A 55 years old man with renal failure presented with
vomiting altered consciousness and fever
pH
pO2
PCO2
HCO3
Na+
ClK+
7.25
70 mmHg
40 mmHg
17 meq/l
140 meq/l
89 meq/l
3.6 meq/l
A. Respiratory acidosis
B. Metabolic Acidosis
C. Metabolic alkalosis +
respiratory acidosis
D. Metabolic acidosis +
Respiratory acidosis
E. D + Metabolic alkalosis
Acid Base Disorders
A ss years old man with renal failure presented with
vomiting and pleuritic chest pain
pH
7.25
pO2
70 mmHg
PCO2
40 mmHg
HCO3
17 meq/l
Na+
140 meq/l
Cl89 meq/l
K+
3.6 meq/l
AG
140-(89+17) =34
D AG = 34-10=24
D HCO3 = 24-17=7
High A-a gradient
Acid Base Disorders
16 years old boy , a case of FSGS on diuretics and
Steroids presented with BP 70/40 mmHg
pH
7.4
PCO2
40 mmHg
HCO3
24 meq/l
Na+
143 meq/l
Cl95 meq/l
K+
3.6 meq/l
S. Albumin 1 gram/dl
A. no acid base
disorder
B. Respiratory acidosis
C. Metabolic alkalosis
+ resp acidosis
D. Metabolic acidosis +
resp alkalosis
E, None of the above
Acid Base Disorders
16 years old boy , a case of FSGS on diuretics and
Steroids presented with BP 70/40 mmHg
pH
7.4
PCO2
40 mmHg
HCO3
24 meq/l
Na+
143 meq/l
Cl95 meq/l
K+
3.6 meq/l
S. Albumin 1 gram/dl
A. no acid base
AG =143-(95+24) = 24
disorder
Corrected
AG=
B. Respiratory
acidosis
24+(4-C.Alb)
* 2.5 =alkalosis
31.5
Metabolic
Delta AG +=resp
21.5acidosis
D. Metabolic
Delta bicarb
= 0 acidosis +
resp
alkalosis
Mixed high
anion
gap
E, None of the above
metabolic acidosis + Alkalosis
Glucose
90 mg/dl
 Urea
30 mg/dl
 Serum Sodium
136 meq/l
 Serum potassium 4 meq/l
 Calc osm
291 mosm/l
 Serum osm
311 mosm/l
 Osmolar gap =20 delta OG=10
 460 mg/l of ethanol or
 320 mg/l of methanol

Acid Base Disorders
HCO3
Na+
ClK+
17 meq/l
140 meq/l
89 meq/l
3.6 meq/l
If delta delta ratio
=1 only high AG
Met Acidosis
Berend K et al. N Engl J Med 2014;371:1434-1445
Berend K et al. N Engl J Med 2014;371:1434-1445
Base Excess

= 0.9287 (HCO3 - 24.4 + 14.83 (pH - 7.4))
Predicted pH = 7.4 + pCO2 * 0.08
 pH = Actual pH – predicted pH
 Base Excess = pH *10/0.15

For each 0.15 unit difference in pH
Base excess or deficit will be =10
Approach to Acid Base Disorders


Traditional or Boston approach
Copen Hagen approach
◦ Base excess

Stewart / Physiochemical approach
◦ PCO2
◦ Non-volatile weak ion acid buffer A Total
 Atotal = A- + AH (Albumin, Pi, SO4, Hb)
◦ Strong ion difference (SID)
 (Na+K+Ca+Mg) – (Cl+Lac)
 = A- + HCO3
 = 40-42

The physiologic or “Boston” method
◦ uses measurements of arterial pH, pCO2, and
[HCO3−] together with an analysis of the anion gap
(AG) and a set of compensation rules.

2. The Base Excess (BE) or “Copenhagen” method
uses
◦ measurements of arterial pH and pCO2, and
calculation of the BE and the AG.

3. The physicochemical or “Stewart” method uses
◦ Measurements of arterial pH and pCO2 together
with the calculated apparent (SIDa) and effective
(SIDe) “Strong Ion Difference,” the “Strong Ion Gap”
(SIG = SIDa-SIDe), and the total concentration of
plasma weak acids (Atot).