Metabolic Acidosis

2. Objectives

3.  A pH imbalance in which the body has accumulated too much acid due to metabolism and
does not have enough bicarbonate to effectively neutralize the effects of acid.
 Characterized by :
-Reduction in serum bicarbonate (HCO3)- concentration
-Decrease in the arterial partial pressure of carbon dioxide (PaCO2)
-Reduction in blood pH < 7.35

4. Blood pH
Normal blood pH = balance between HCO3- and CO2 = 7.35 – 7.45

5. Ischemia O2
Pyruvate
TCA
Glycolysis
Glucose
Lactate
Acetyl-coA
(Anaerobic
Metabolism)
O2
Pathophysiology

6. Lactate
Pathophysiology Process (Cont.)
H+
Tissues
(Anaerobic
Metabolism)
H+ + HCO3-(Blood)
H2 Co3
H2O
+Co2

7. Anion Gap
BLOOD NEEDS TO REMAIN ELECTRICALLY NEUTRAL
Total number of Cations (+) = Total number of Anions
[ (Na) + (K-) + Unmeasured Cations] – [ (Cl-) + (HCo3-) + Unmeasured Anions ]

8.  This is because there are certain Unmeasured
anions like Phosphates, Sulfates, Urolactic Acid
and Ketone Bodies which are the Unmeasured
anions in case of Pathology.
 Normally it is because of Phosphates and Sulfates
and also Albumin place a very important role in
formation of Anion Gap.
Reason for Anion Gap

9. ANION GAP = [Na+] – [ (Cl-) + (HCO3-)
Ie. Cation – Anion
= 141 - (105 – 24)
= 141 - 129
= 12 meq/L.
NORMAL ANION GAP = 12 meq/L
= +4 for K+
NORMAL RANGE FOR ANION GAP = 8 – 16 meq/L
How do we calculate Anion Gap?

11. INCREASE IN ORGANIC ACID
Organic acids causing high ANION GAP ACIDOSIS :
 Lactic Acid
 Ketoacids (Acetoacetic Acids , Beta hydroxybutyrate
 Formic Acid (Methanol)
 Oxalic Acid (Ethylene Glycol)
HIGH ANION GAP METABOLIC ACIDOSIS

12. Causes of high Anion Gap Acidosis
I)Toxins / Drugs :
- Methanol Poisoning
- Ethylene Poisoning
- Paraldehyde
- Aspirin
II)Ketoacidosis :
- DKA
- Starvation
- Alcohol
III)Lactic Acidosis
IV)Acute Renal Failure

13. 1) Diarrhea
2) Renal Tubular Acidosis
- Most common type : Decreased Bicarbonate
3) Reabsorption in a distal convoluted Tubules.
4) Hyperchloremia : It can occur when water
losses exceed Sodium and Chloride losses
5) Adrenal Insufficiency
CAUSES OF NORMALANION GAP ACIDOSIS
GIT CAUSES :
- Diarrohea
- Enterocutaneous Fistula
- Ureterosigmoidostomy
- Pancreatic Fistula
RENAL CAUSES:
- Renal Tubular Acidosis
- Hypoaldosteronism
- ACE Inhibitors
- Aldosterine Agonist
- Carbonic Anhydrase
Inhibitor

14. SIGNS &
SYMPTOMS

15. Any disturbance of Co2 is Respiratory
Any disturbance of HCO3 is Metabolic
GAIN OF ACID – ACIDOSIS
LOSS OF ACID – ALKALOSIS
GAIN OF ALKALI – ALKALOSIS
LOSS OF ALKALI - ACIDOSIS
Remember

16. BASIC CONCEPT :
 NORMAL pH = 7.35 -7.45
Avg = 7.40
Anything above 7.40 will be Alkalosis
Anything below 7.40 will be Acidic
 NORMAL HCO3- = 22 – 28meq
Avg = 24
 paC02 = 35 – 45mmHg
 paO2 = 70 – 100mmHg
ARTERIAL BLOOD GAS

17. Arterial
Blood Gases

18. COMPONENTS OFABG:
1)Ph
2)Partial CO2 Level
3)Total CO2 Level (tCO2 or HCO3)
4)Partial Pressure of oxygen (PO2)
5)Oxygen saturation
Arterial Blood Gas

19. Compensation of Metabolic Acidosis
 Hyperventilation to decrease the arterial pCo2
-KUSMAUL’s BREATHING also k/a ACIDOTIC BREATHING
 Maximal Compensation takes 12 to 24 hours
- The chemoreceptors inhibition acts to limit and delay the full
ventilatory response until Hco3- shifts and have stabilized across the blood
brain barrier.
- The increase in ventilation usually starts within minutes and is
usually well advanced at 2 hours of onset but maximal compensation may take
12 to 24 hours to develop.
- This is maximal compensation rather than full compensation as it
does not return the extra cellular pH to normal.

20. - Inversely proportional to the amount of H+ ions.
- H+ Ions =
Effects on Physiological Activities
 CONTRACTILITY
 RESPONSE TO
CATECHOLAMINES
 METABOLISM OF
MEDICATIONS
pH is the 1st component of blood sample that is analysed
ACID BASE BALANCE - PH
pH

21. ACID BASE BALANCE – Co2
 PCo2 is a respiratory component of acid-base balance
 Co2 is transported in Hb and dissolves in plasma
 pH changes to SAME degree but opposite direction
 Co2 level in blood cells will lead to ACIDOSIS
 Conversely ed level of Co2 in blood will lead to ALKALOSIS
 Co2 + H2O H2 Co3
 H2 Co3 pH = Acidic Condition

22. ACID BASE BALANCE – BICARBONATE
 Range HCo3  22-26meq/l
 HCo3 are physiological buffers maintained by the kidneys to attain
normal pH
 HCo3 outside the normal range usually found by metabolic changes in
Acid-base balance

23. Case I
pH- 7.21, HCo3- - 10, pCo3-40
pH - ed
HCo3- - ed
c/o – Acute Metabolic Acidosis
(Reason for Acute: pH- reduced, paCo2- Normal)
“A Friend in need is a friend indeed”
Rate and depth of breathing  KUSMAUL’S BREATHING
Now,
pH  7.30  7.40
HCo3  14  17
pCo3  36  31
Therefore, Aim to attend pH – 7.40 Achieved

24. Case II
pH – 7.60 ; HCo3 – 70 ; paCo2  40
C/O Metabolic Alkalosis
Rate and depth of breathing will go down (SHALLOW
BREATHING)
Now,
paCo2  46  51
HCo3-  62  59
pH  7.50  7.40

25. Case III
 If measured HCo3- is 12mmol/L , then the expected pCo2 (at maximal compensation)
would be : (1.5* 12) + 8
= 18+ 8
= 26 mmHg
 If the actual pCO2 was within +/- 2mmHg of this (And 12 to 24 hours have past from
onset) then the respiratory compensation has reached its maximal value.(And there
would be no evidence of primary respiratory acid-base disorder.)
 If pCo2 was 40mmHg  markedly different from the expected value of 26mmHg and
indicates the presence of quite a marked second primary acid-base disorder.

26. Maintaining Hyperventilation in ventilated patients
 Ventilation should set to mimic the compensatory hyperventilation to keep the pCo2
low.
 If ventilation is set to some standard value and the pCo2 allowed to rise towards
40mmHg, then this represents the imposition of an Acute Respiratory acidosis and pH
can fall rapidly.
 Co2 crosses cell membranes readily so intracellular pH falls rapidly also, resulting in
depression of Myocardial Contractility, Arrythmias and a rise in Intrarenal pressure.
 The patient may deteriorate soon after intubation and ventilation and the medical ST.

27. Thank you