This document discusses acid-base physiology and disorders. It provides details on: 1. Factors that determine pH levels in the body and how acids are neutralized through the Henderson-Hasselbalch equation. 2. Types of acid-base disorders including metabolic acidosis/alkalosis from accumulation or depletion of acids, and respiratory acidosis/alkalosis from accumulation or depletion of carbon dioxide. 3. Methods for evaluating acid-base disorders including anion gap, delta gap, urine anion gap and calculating compensation based on the Boston method. 4. Treatment approaches for correcting the underlying causes of different acid-base imbalances.

1. ACIDOSIS AND
ALKALOSIS
Dr. Ubaidur Rahaman
M.D. (Internal Medicine), EDIC
Internist and Critical Care Specialist

2. “Life is struggle,
not against sin, not against money power….
but against Hydrogen ion.”
- H .L. MENCKEN

3. 1952, Polio Epidemic
Blegdam Hospital, Copenhagen, Denmark
Bjorn Ibsen, Anesthesiologist
Manual bag ventilation
1500 Medical and Dental students, 24/7 shift of 6-8 hours 1,65,000 hours

4. 1831: O’ SHAUGHNESSY
1903: ARRHENIUS

5. ACID BASE PHYSIOLOGY IN BODY
Solution- H2O ; 60% of body weight
H2O↔ H+
+ OH-
All H+
are derived from water dissociation
pH : ICF= 6.8-7.0, ECF= 7.4
ICF- relatively impermeable to ionic material,
pH remains constant despite dramatic change in ECF pH
ECF- pH affected due to fluid, electrolytes and CO2

6. FACTORS DETERMINING [H+] OF ECF

7. MAJOR SOURCES OF ACIDS IN BODY
CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3-CO2
dHb-histidine residue
Cl
Haldane
effect
Chloride shift
CO2 also buffered directly by Hb and plasma proteins
Also carried in dissolved form
VOLATILE ACID-CO2

8. MAJOR SOURCES OF ACIDS IN BODY
METABOLIC ACIDS: LACTIC, KETO, SO4
-
, PO4
-

9. CO2 + H2O ↔ H2CO3↔ H+ + HCO3-
IMBALANCE IN PRODUCTION AND ELIMINATION RESULTS IN ACIDOSIS OR ALKALOSIS
METABOLIC ACIDS AND VOLATILE ACIDS ARE CONTINUOUSLY BEING FORMED IN BODY AS
END PROT OF METABOLISM AND CELLULAR RESPIRATION,
AND CONTINUOUSLY BEING EXCRETED OR EXHALED
TO MAINTAIN HOMEOSTASIS
IN RESPONSE TO ACIDOSIS OR ALKALOSIS
HOMEOSTASIS IS GOVERNED BY FOLLOWING FUNDAMENTAL EQUATION

10. WHAT NEUTRALIZES THESE
ACIDS
H2O + CO2↔ H2CO3 ↔ H+
+ HCO3
-
HCO3
-
WILL RISE/ FALL
BY SAME AMOUNT AS
LOSS/ GAIN IN H+

11. H2O + CO2↔ H2CO3 ↔ H+
+ HCO3
-
TO MAINTAIN EQUILIBRIUM

12. COMPENSATION
WHEN A PRIMARY ACID-BASE DISORDER EXISTS,
THE BODY ATTEMPTS TO RETURN THE PH TOWARDS NORMAL,
SO THAT ENZYMATIC ACTIVITY IS NOT HAMPERED

13. METABOLIC ACIDOSIS
EXP PaCO2= 1.5 × HCO3 + 8 ± 2
METABOLIC ALKALOSIS
EXP PaCO2= 0.7 × HCO3 + 21 ± 2
RESPIRATORY ACIDOSIS
Acute – EXP HCO3= 24+[(PaCO2-40) × 1/10]
Chronic – EXP HCO3= 24+[(PaCO2-40) × 4/10]
RESPIRATORY ALKALOSIS
Acute - EXP HCO3= 24-[(40-PaCO2) × 2/10]
Chronic- EXP HCO3= 24-[(40-PaCO2) × 5/10]
COMPENSATION CALCULATION USING BOSTON APPROACHCOMPENSATION CALCULATION USING BOSTON APPROACH

14. H2O + CO2↔ H2CO3 ↔ H+
+ HCO3
-
ACIOSISALKALOSIS
METABOLIC RESPIRATORY
TO MAINTAIN EQUILIBRIUM

15. H2O + CO2↔ H2CO3 ↔ H+
+ HCO3
-
METABOLIC ACIDOSIS: ACCUMULATION OF METABOLIC ACID

16. H2O + CO2↔ H2CO3 ↔ H+
+ HCO3
-
METABOLIC ALKALOSIS: DEPLETION OF METABOLIC ACID

17. H2O + CO2↔ H2CO3 ↔ H+
+ HCO3
-
RESPIRATORY ACIDOSIS: ACCUMULATION OF VOLATILE ACID

18. H2O + CO2↔ H2CO3 ↔ H+
+ HCO3
-
RESPIRATORY ALKALOSIS: DEPLETION OF VOLATILE ACID

19. [H+
] = 24 × pCO2/ [HCO3
-
]
pH = 6.1 + log [HCOpH = 6.1 + log [HCO33
--
]/[pCOpCO22 × 0.03 ]× 0.03 ]
pCO2 HCO3
-
Low Low
High High
pH
Low High
Metabolic Acidosis Respiratory
Alkalosis
Respiratory
Acidosis
Metabolic Alkalosis
Both pCO2 and HCO3
-
move in same direction for a given acid base disorder
pH is determined by ratio of pCO2 and HCO3
-

20. 1909 – HENDERSON’S EQUATION
Hydrogen ion concentration is determined by ratio of CO2 and HCO3
-

21. pH scale: pH = -log [H+ ]pH scale: pH = -log [H+ ]
1912 – SORENSON
Normal [H+
] is 40 neq/L (4 × 10-8
or 0.000000004)
Normal pH is 7.4

22. HENDERSEN HASSELBALCH EQUATIONHENDERSEN HASSELBALCH EQUATION
pH is determined by ratio of pCO2 and HCO3
-

23. THESE FACTORS MUST OBEY THREE DISTINCT
LAWS

24. THEREFORE

25. BASED ON LAW OF ELECTRONEUTRALITY
A- (WEAK ACIDS)
Albumin, Pi
UMA (UNMEASURED ANIONS)
unmeasured strong anions
(lactate, keto ions)
UNDER NORMAL PHYSIOLOGY UMA ARE NEGLIGIBLE
AS CONTINUOUSLY METABOLIZED/ EXCRETED

26. BASED ON LAW OF ELECTRONEUTRALITY

27. BASED ON LAW OF ELECTRONEUTRALITY
A- (WEAK ACIDS)
Albumin, Pi
}
UMA (UNMEASURED ANIONS)
unmeasured strong anions
(lactate, keto ions)

28. BASED ON LAW OF ELECTRONEUTRALITY
Lactic/ keto acidosis= UMA
AG> 16
AG= [Na+K+Mg+Ca ] – [Cl+ SO4+PO4+HCO3
-
]
} = A + UMA
Normal AG= 12 ± 4= A-
UMA= 0
ACID ACCUMULATION
AG= [Na] – [Cl+HCO3
-
]
As Na and Cl are major ions in ECF, other ions can be negated

29. BASED ON LAW OF ELECTRONEUTRALITY
} Normal SID= 40 ± 4
UMA= 0
= BB= AG+ HCO3
-
= 12 ± 4 + 24

31. AG= [Na ] – [Cl+HCO3
-
]
HIGH AG
METABOLIC ACIDOSIS
NORMAL AG
METABOLIC ACIDOSIS
A-
UMA
HCO3
-
Measure
d
anions
[Cl]

33. AG= [Na ] – [Cl+HCO3
-
]
DELTA GAP OR GAP GAP

34. AG= [Na ] – [Cl+HCO3
-
]
DELTA GAP OR GAP GAP

35. AG= [Na ] – [Cl+HCO3
-
]
DELTA GAP OR GAP GAP

36. DELTA GAP OR GAP GAP
ratio of
AG excess / deficit in HCO3 = 1
ratio of
AG excess / deficit in HCO3 < 1
ratio of
AG excess / deficit in HCO3 > 1
coexistant
NAG Met acid
coexistant
Met Alk

37. URINE ANION GAP
(UAG)
normal UAG = 0
UAG becomes negative
( -20 to -50 meq/L)
UAG remains
positive or slightly negative

39. METABOLIC ACIDOSIS: TREATMENT
CORRECTION OF ETIOLOGY

41. METABOLIC ALKALOSIS:
ETIOLOGY

42. METABOLIC ALKALOSIS:
ETIOLOGY

43. METABOLIC ALKALOSIS:
ETIOLOGY

44. METABOLIC ALKALOSIS: MANAGEMENT
CORRECTION OF ETIOLOGY

45. CO2 NARCOSIS
DECREASED LOC, HYPERTHERMIA, HYPERTENSION, BOUNDING PULSES, PERSPIRATION

46. RESPIRATORY ACIDOSIS: MANAGEMENT
CORRECTION OF ETIOLOGY

47. TREMORS, TINGLING, NUMBNESS, HYPOTENSION, TACHYCARDIA, HYPOTHERMIA, ALTERED LOC, SEIZURES

48. RESPIRATORY ACIDOSIS: MANAGEMENT
CORRECTION OF ETIOLOGY

49. Acid-base analysis: a critique of the Stewart and bicarbonate-centered approaches
Ira Kurtz, Jeffrey Kraut, Vahram Ornekian and Minhtri K. Nguyen
Am J Physiol Renal Physiol 294:F1009-F1031, 2008

50. THANK YOU
"Stay committed to your decisions,
but stay flexible in your approach”
Tom Robbins

51. • Buffer Base: Singer- Hastings 1948
• Boston approach (CO2-HCO3): Schwartz
• CopenHagen Approach (BE): Siggard-Anderson 1948
• Anion Gap approach: Emmet and Narins

52. • There has been considerable discussion over the past 30 years about the merits
and demerits of the BDE compared with the CO2-HCO3 system. In reality, there is
little difference between the two; both equations and nomograms were derived
from in vivo patient data and abstracted backward. Consequently, for most
patients, either approach is relatively accurate but misleading. Using measures of
buffer base as a means of quantifying acid-base disturbances does not allow the
clinician to distinguish between acidosis caused by lactate or chloride or alkalosis
caused by dehydration or hypoalbuminemia. These measures may miss the
presence of an acid-base disturbance entirely; for example, a hypoalbuminemic
(metabolic alkalosis), critically ill patient with a lactic acidosis may have a normal-
range pH, bicarbonate, and base excess. This may lead to inappropriate or
inadequate therapy.