Acid-Base Balance

Presented by :
Rachmat Hidayat, S.Ked
Frizky Arlind, S.Ked
1. Basic Concepts


[H
+
] ~ [PCO
2
/HCO
3
]
2. Compensatory Response
Primary Disorder Compensatory Response
PCO
2

Respiratory acidosis
HCO
3
Metabolic alkalosis
PCO
2
Respiratory alkalosis
HCO
3
Metabolic acidosis
HCO
3
Metabolic acidosis
PCO
2
Respiratory alkalosis
HCO
3
Metabolic alkalosis
PCO
2
Respiratory acidosis
3. The Rules of Acid Base Interpretation
Rule 1: A primary metabolic disorder is present if :
a. pH and PCO
2
change in the same direction, or
b. pH is abnormal but PCO
2
is normal

Rule 2 : The following equation will identify an associated
respiratory disorder :
a. For metabolic acidosis
expected PCO
2
= 1,5 (HCO
3
) + 8 (2)
b. For metabolic alkalosis
expected PCO
2
= 0,7 (HCO
3
) + 20 (1,5)
If PCO
2
is higher than expected, then there is an associated respiratory
acidosis and if PCO
2
is lower than expected, there is an associated
respiratory alkalosis
Cont
Rule 3 : A primary respiratory disorder
is present if pH and PCO
2
change in
opposite directions.

Rule 4: The relationship between the
change in PCO
2
and the change in pH
can be used to identify an associated
metabolic disorder or an incomplete
compensatory respons.
a. for respiratory acidosis
acute uncompensated acidosis;
pH changes 0,008 units for
every 1mmHg change in PCO
2
.
chronic compensated acidosis;
pH changes 0,003 units for
every 1 mmHg changes PCO
2
.

Change in
pH/PCO
2

Disorder
Above 0,008 Associated
metabolic
acidosis
0,003 to 0,008 Partially
compensated
respiratory
acidosis
Below 0,003 Associated
metabolic
alkalosis
Cont..
B. for respiratory alkalosis
acute uncompensated
alkalosis; the pH/PCO
2

change is the same as
for acute respiratory acidosis
(0,008).
chronic compensated
alkalosis; the serum pH
change 0,017 units for
every 1 mmHg change in
PCO
2
.


Change in
pH/PCO
2
disorder
Above 0,008 Associated
metabolic
alkalosis
0,002 to 0,008 Partially
compensated
respiratory
acidosis
Below 0,002 Associated
metabolic
acidosis
Cont.
Rule 5 : A mixed metabolic-respiratory disorder
is present if pH is normal and PCO
2
is abnormal
4. Acid-Base Disorders
4.1. Respiratory Acidosis
alveolar hipoventilation
(CNS depression, cerebral ischemia,chest
Wall abnormalities, COPD, severe asthma)

Respiratory acidosis
(increased PCO
2
)



increased CO
2
Production
(malignant hyperthermia, shivering, thyroid storm)

Compensatory Respon for Respiratory Acidosis
Renal compensation during acidosis ;
1. Increased Reabsorption of HCO
3


Cont
2. Increased Excretion of Titratable Acids

Cont
3. Increased Formation of Ammonia

Treatment of Respiratory Acidosis
1. Increasing alveolar ventilation


2. Reducing CO
2
production

4. Acid-Base Disorders
4.2. Metabolic Acidosis
Metabolic acidosis
Normal anion gap High anion gap
Cont..
Normal Anion Gap High Anion Gap
diare 1. laktatacidosis
renal insufficiency 2. ketoacidosis
infus chloride 3. renal failure
Compensation of 4. Salicylates
alkalosis respirasi
ureterosigmoidostomy
renal tubular asidosis
Cont
Serum Anion Gap
Unmeasured Anions (UA) Unmeasured Cations (UC)

Protein 15mEq/L K 4,5 mEq/L
PO4 2 Ca 5,0
SO4 1 Mg 1,5
Organic acid 5
Total 23 Total 11

Anion gap: UA-UC= 12 mEq/L
UA + (Cl + HCO3) = Na + UC
UA-UC = Na (Cl + HCO3)
Cont..
Urin Anion Gap
Total anion = total kation
UA + Cl = Na + K + UC
Anion gap: UA-UC = (Na + K) Cl

Urine anion gap Urine pH Diagnosis
negatif < 5,5 normal
positif > 5,5 RTA
negatif > 5,5 diare

Urine anion gap is used to identify a defect in renal tubular acidification
(RTA) in patient with hyperchloremic (normal anion gap) metabolic
acidosis.
Cont.
Strong acid nonvolatile H
+
+ anion


+ HCO
3
Accumulate

H
2
O + CO
2
High anion gap


Acid




Cont.
Gastrointestinal disorder

RTA ( HCO
3
)
Cl Hyperchloremic acidosis
NaCl infusion
normal anion gap
Amino acid infusion
Cont..
Treatment of
metabolic acidosis
Empirically 1 mEq/kgBB


NaHCO
3




Bicarbonat space

NaHCO
3
= base defisit x bicarbonat space x body weight

Bicarbonat space: 25% - 60% of body weight
Anesthetic Consideration in Patients with Acidosis
Acidemia can potentiate the depressant effects of most sedatives
and anesthetic agents on the central nervous and circulatory
systems. Because most opioids are weak bases, acidosis can
increase the fraction of the drug in the nonionized form and facilitate
penetration of the opioid into the brain. Increased sedation and
depression of airway reflexes may predispose to pulmonary
aspiration. The circulatory depressant effects of both volatile and
intravenous anesthetics can also be exaggerated. Moreover, any
agent that rapidly decreases sympathetic tone can potentially allow
unopposed circulatory depression in the setting of acidosis.
Halothane is more arrhythmogenic in the presence of acidosis.
Succinylcholine should generally be avoided in acidotic patients with
hyperkalemia to prevent further increases in plasma [K+]. Lastly,
respiratorybut not metabolicacidosis augments nondepolarizing
neuromuscular blockade and may prevent its antagonism by
reversal agents.

4. Acid-Base Disorders
4.3. Respiratory Alkalosis
Central stimulation
(Pain, anxiety, ischemia, stroke
Tumor, infection, fever)

CO
2
Respiratory alkalosis



Peripheral stimulation
(Hypoxemia, pulmonary disease, asthma)
Cont.
Treatment respiratory alkalosis


Correction of underlying process
4. Acid-Base Disorders
4.4. Metabolic Alkalosis
Chloride sensitive
(gastrointestinal, vomiting, chloride
Diare, diuretics)


HCO
3
Metabolic alkalosis

Chloride resistant
(increased mineralocorticoid activity,
Hyperaldosterinism, severe hypokalemia)
Cont..
Chloride sensitive metabolic alkalosis:

Depletion extracellular fluid

Na reabsorb increase

Cl not enough to accompany
with all Na reabsorb

increased H
+
secretion HCO
3




Hypokalemia







Cont.
Chloride Resistant Metabolic Alkalosis:


Increased mineralokortikoid activity

Na retention, expansion of extracelullar fluid volume

Increased H and K secretion


HCO
3
Cont.
Treatment of metabolic alkalosis:

Chloride sensitive Chloride Resistant


Intravenous NaCl aldosteron antagonis
(spironolactone)
Anesthetic Consideration in Patients with Alkalemia



Respiratory alkalosis appears to prolong the duration of opioid-
induced respiratory depression; this effect may result from increased
protein binding of opioids. Cerebral ischemia can occur from marked
reduction in cerebral blood flow during respiratory alkalosis,
particularly during hypotension. The combination of alkalemia and
hypokalemia can precipitate severe atrial and ventricular
arrhythmias. Potentiation of nondepolarizing neuromuscular
blockade is reported with alkalemia but may be more directly related
to concomitant hypokalemia.


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