Acid Base Disturbance

Teguh Santoso
Introduction
1887 : Arrhenius :
acid = hydrogen (H
+
) ion donor
base = hydroxyl (OH
-
) ion donor

1948 : Singer and Hastings
buffer base (BB) = a quantitative index of the surplus amount of fixed acid
or base in the blood

1960 : Astrup
standard bicarbonat or base excess should be used as an index of the
nonrespiratory acid-base status of the blood.
Henderson-Hasselbach : pH depends on the interaction of carbondioxide and
bicarbonat

1983 : Stewart
SID (strong ion difference), based on electroneutrality and mass conservation

(Ferrer L. 2006. Critical Care Medicine)
Arterial Blood Gases
Obtaining ABGs
ABGs are valuable only if
obtained properly and measured carefully

stable FiO
2
for at least 10 minutes
body position supine = SpO
2
worse
ventilatory pattern RR/ depth ~ PaCO
2
/PaO
2

prolonged attempt pain/hyperventilation
Pitfalls in
Collection, Analysis, and Interpretation
Timing of analysis : do not delay
PaCO
2
rises 3 10 mmHg/hour in un-iced specimens
PaO
2
remains stable in an iced sample for 1 2 hr
Pseudohypoxemia
diffusion of O
2
through the wall of plastic syringes may lead to
false reduction in measured PaO
2
Pseudoacidosis
excessive amounts of acidic heparin in the sampling syringe may
cause pseudoacidosis by diluting and/or neutralizing serum
bicarbonate
Air bubbles
room air : PO
2
= 150/PCO
2
= 0 when large air bubbles are
mixed with arterial blood PaO
2
rises/PaCO
2
falls
Contamination of arterial samples with venous blood
Basic ABG Concepts
Normally,
arterial pH 7,35 7,45

Breathing room air :
PaCO
2
35 45 mmHg
PaO
2
> 80 90 mmHg

Venous blood gases :
lower pH (~ 7,35)
PvO
2
~ 40 mmHg
PvCO
2
~ 45 mmHg
Buffer System
Carbonic acid : CO
2
,
HCO
3
-

Noncarbonic : albumin,
hemoglobin, phosphat,
bone carbonates
Compensatory
mechanism : renal,
respiratory
Acid-Base Derangements
Terminology of acid-base disorders
acidemia and alkalemia refer to blood pH,
acidemia = blood pH < 7.35
alkalemia = blood pH > 7.45
acidosis and alkalosis refer to basic
pathophysiologic processes or tendencies
favoring the development of acidemia or
alkalemia
Stepwise ABG Analysis
Henderson-Hasselbach approach
1. pH is analyze first :
pH < 7.35 = acidemia
pH > 7.45 = alkalemia
pH normal ?
+ no acid-base disorder
+ acid-base disorders with perfectly offsetting
pH effects exist
+ near complete physiologic compensation
Henderson-hasselbach
2. In the acidemic patient,
an elevated PaCO
2
indicates that some component of
respiratory acidosis is present.
bicarbonat concentration can be used to decide
whether appropriate compensation is occurring or if
concurrent metabolic disorder is present :
|HCO
3
|

= | (0.10 0.35) unit ~ | PaCO
2

appropriate metabolic compensation.
lesser | |HCO
3
|

complicating metabolic acidosis
or insufficient time to compensate.
greater | |HCO
3
|

super imposed metabolic
alkalosis
Henderson-Hasselbach
3. In acidemic patient
a reduced PaCO
2
indicates metabolic acidosis
Diagnosis is reached by comparing the observed PaCO
2
to
that predicted by directly measuring the serum HCO
3
content.
the expected PaCO
2
= (1.5 x HCO
3
) + (8 2)
| 1.0 1.3 mmHg PaCO
2
~ change in 1 mEq HCO
3

if : observed PaCO
2
= expected value
simple metabolic acidosis +
appropriate respiratory compensation
PaCO
2
> expected value
respiratory + metabolic acidosis

Henderson-Hasselbach
4. In the alakalemic patient,
a low PaCO
2
diagnoses respiratory alakalosis
reduction in |HCO
3
| of 0.2-0.5 x change in
PaCO
2
compensation
failure to lower HCO
3
by

> 0.2 x change in
PaCO
2
superimposed metabolic alkalosis
HCO
3
that declines > 0.5 x change in PaCO
2

a component of metabolic acidosis
Expected compensation for acid-base disorders
Primary
disorder
Primary
change
Compensatory
change
Expected compensation
Metabolic
acidosis
+ HCO
3
+ PaCO
2

APaCO
2
= 1.2 AHCO
3

Metabolic
alkalosis
| HCO
3
| PaCO
2


A PaCO
2
= 0.9 AHCO
3
Respiratory
acidosis
| PaCO
2
| HCO
3

Acute
Chronic
AHCO
3
= 0.10 APaCO
2
AHCO
3
= 0.35 APaCO
2
Respiratory
alkalosis
+ PaCO
2
+ HCO
3


Acute
chronic
AHCO
3
= 0.2 APaCO
2

AHCO
3
= 0.5 APaCO
2

N
Metabolic Alkalosis
Uncompensated
Metab. Alk
Resp. Alkalosis
Metabolic Acidosis
Respiratory Acidosis
Stewart Approach (Strong Ion Difference)
Three components in biological fluids are
subjected to these principals :
1. water, weakly dissociated into H
+
and OH
-

2. strong ions, completely dissociated
such as Na
+
, K
+
, Cl
-
and certain molecules or
compounds such as lactate
3. weak acids, incompletely dissociated
compounds
Stewart strictly distinguished between dependent
and independent variables in accord with these
principles
Dependent variables can only change if
independent variables allow this change
(changes in pH, H
+
and HCO
3
are only possible if
either SID or ATOT itself changes)
Dependent variables
bicarbonate
pH
H
+

Independent variables
pCO
2
weak acid (ATOT)
strong ion difference
(SID)

Strong ion difference
In healthy humans,
the normal SID is 40
42 mEq/lt
SID < 40 relates to
metabolic acidosis
SID > 42 indicates
metabolic alkalosis
SID = (Na+K+Ca+Mg)
(Cl + lactate)
SID = |Na+K| - |Cl|

Na
+


K
Ca
Mg
Cl
-


P
Alb
HCO
3

UA