This document provides an overview of acid-base physiology, including: - Definitions of acids, bases, and acid-base balance - The three main systems that maintain pH balance: buffers, respiration, and renal - The four basic types of acid-base imbalances: metabolic acidosis, metabolic alkalosis, respiratory acidosis, respiratory alkalosis - Details on specific disorders like respiratory acidosis, metabolic acidosis, and mixed disorders - Compensatory responses and interpretation of blood gas measurements - Case studies on mixed disorders involving respiratory and metabolic components In under 3 sentences, it summarizes key concepts in acid-base physiology and provides examples of interpreting acid-base imbalances.

1. 1

2. Contents
Basics
Normal Physiology
Abnormalities
Respiratory Acid Base Disorders
Metabolic Acid Base Disorders
Case study
2

3. ACID AND BASE
 Acid
Any compound which forms H⁺ ions in solution
(proton donors)
eg: Carbonic acid releases H⁺ ions
 Base
Any compound which combines with H⁺ ions in
solution (proton acceptors)
eg: Bicarbonate(HCO3⁻) accepts H+ ions
 Acids and bases can be Strong or Weak
3

4. ACID–BASE BALANCE
 Normal pH : 7.35-7.45
 Homeostasis of pH is tightly controlled
Extracellular fluid = 7.4
Blood = 7.35 – 7.45
< 6.8 or > 8.0 death occurs
 If any of these changes causes the pH to change to a value
outside the normal range, the suffix emia is used to describe
the acid-base derangement:
 Acidosis (acidemia) below 7.35
 Alkalosis (alkalemia) above 7.45
4

5. 3 SYSTEMS THAT MAINTENANCE PH
5
• Moves or release hydrogen ions
1. Buffers
• Regulate carbonic acid by eliminating or retaining
CO2
2. Respiratory system
• Long term regulation of acid-base in body by
regulating bicarbonate ions.
3. Renal system

6. 1. BUFFER SYSTEMS
 Chemical buffers are available in extracellular/ intracellular
compartments
• Phosphate
• Protiens
• bicarbonate
 Helps to maintain a stable pH , Removes or release H+
ions
• Excess acid (acidosis) pH <7.35, buffers bind with H+
ions
• Too alkaline (alkalosis) pH >7.45, buffers release H+
ions
6

7. Bicarbonate system constituted of plasma sodium
bicarbonate (NaHCO3) and carbonic acid (H2CO3) and
cellular H2CO3 and potassium bicarbonate (KHCO3)
extracellular space
The phosphate system found in renal tubular fluid and
intracellularly
Proteins intracellular spaceMostl powerfull in
Most dominating in
7
Three buffering systems

8. 2. RESPIRATORY SYSTEM
 Normal PaCO2 = 35- 45 mmHg
 Pulmonary buffering system is as effective as the chemical
buffering system . The lungs respond to deviations in pH by
altering the rate and depth of ventilation. Eliminates or retains
carbon dioxide
 ↑ carbon dioxide (acid) stimulate respiration
↑rate & depth of resp ↓ pH to normal range
 Alkalosis depresses respiration
↓ rate & depth of resp retains carbon dioxide
8

9. The kidneys are the third line of defence against wide
changes in body fluid pH
• movement of bicarbonate
• Retention/Excretion of acids
• Generating additional buffers
Long term regulator of ACID – BASE balance
May take hours to days for correction
3. Renal System
9

10.  Role of kidneys is
preservation of body’s
bicarbonate stores
• by controlling
serum bicarbonate
concentration
through the
regulation of H+
excretion
• bicarbonate
reabsorption
• production of new
bicarbonate
 Proximal
tubule: 70-
90%
 Loop of Henle:
10-20%
 Distal tubule
and collecting
ducts: 4-7%
RENAL
REABSORPTION
OF BICARBONATE
i. MAINTAIN BICARBONATE
10

11.  Regeneration of titrated bicarbonate by
excretion of:
• Titratable acidity (mainly phosphate)
• Ammonium salts
ii. Regeneration Of Bicorbonate
11

12. • TITRATABLE ACIDITY
 Occurs when secreted H+
encounter & titrate phosphate
in tubular fluid
 Refers to amount of strong
base needed to titrate urine
back to pH 7.4
 40% (15-30 mEq) of daily
fixed acid load
12

13. • AMMONIUM EXCRETION
 Occurs when secreted H+
combine with NH3 and are
trapped as NH4
+ salts in tubular
fluid
 60% (25-50 mEq) of daily fixed
acid load
 Very adaptable (via
glutaminaseinduction)When
blood acidity is significantly
increased, glutamine
metabolized into ammonia.
 Ammonia→ recipient of H+.
13

14.  Normal bicarbonate 22-26 mEq/L
 Acidosis
• Excess H+ ions
• pH falls
• kidneys excrete H+ and retain bicarbonate
 Alkalosis
• Less H+ ions
• pH increases
• Kidneys retains H+ ions & excrete bicarbonate
Interactions Among The Carbonic Acid–
bicarbonate Buffer System And Compensatory
Mechanisms In The Regulation Of Plasma pH
14

15. Interactions among the Carbonic Acid–Bicarbonate Buffer System
and Compensatory Mechanisms in the Regulation of Plasma pH
15

16. HENDERSON-HASSELBACH EQUATION
 pH = pKa + log([HCO3
-]/.03xpCO2)
 Shows that pH is a function of the ratio between
bicarbonate and pCO2
 PCO₂ - ventilatory parameter (40 +/- 4)
 HCO₃⁻ - metabolic parameter (22-26 mmol/L)
  


3
2
24
HCO
PaCO
H
Kassirer-Bleich equation
16

17. ACID–BASE MONITORING
 Acid–base status can be monitored intermittently or
continuously.
 Arterial blood gas (ABG) analysis remains the gold
standard in assessing for acid–base disorders.
 In the ICU, ABGs can be obtained by arterial
puncture or through an indwelling arterial catheter
17

18. GETTING AN
ARTERIAL BLOOD
GAS SAMPLE
18

19. SAMPLE ANALYSIS
 The blood gas machines in most labs actually
measure the pH ,the pCO2 and the pO2.
bicarbonate level -------- from a serum sample.
 The [HCO3-] and the base difference are calculated
values using the Henderson-Hasselbalch equation.
19

20. INTERPRETATION OF BLOOD GAS
MEASUREMENTS
 It is an easy mathematical exercises
 immediately and rapidly get a insight into the underlying
process causing the disturbance in acid–base status.
20

21.  Acidosis “is a disorder that predisposes/lead to low
systemic pH. Utilizing the Henderson–Hasselbalch
equation, this can be caused by a fall in systemic
bicarbonate concentration or by an elevation in the
pCO2 .
 Alkalosis is a disorder that predisposes/lead to high
systemic pH. This is usually caused either by an
increase in systemic bicarbonate concentration or by
a fall in the pCO2. 21

22. 22

23. FOUR BASIC TYPES OF IMBALANCE
Metabolic Acidosis
Metabolic Alkalosis
Respiratory Acidosis
Respiratory Alkalosis
23

24. A change in either the PCO2 or the HCO3 will cause a change
in the pH of extracellular fluid.
When the change involves the PCO2, the condition is called a
respiratory acid-base disorder: an increase in PCO2 is a
respiratory acidosis, and a decrease in PCO2 is a respiratory
alkalosis.
When the change involves the HCO3, the condition is called a
metabolic acid-base disorder: a decrease in HCO3 is a
metabolic acidosis, and an increase in HCO3 is a metabolic
alkalosis.
Acid Base Disorders
24

25. ACID BASE DISORDERS
Disorder pH [H+] Primary
disturbance
Secondary
response
Metabolic
acidosis
   [HCO3
-]  pCO2
Metabolic
alkalosis
   [HCO3
-]  pCO2
Respiratory
acidosis
   pCO2  [HCO3
-]
Respiratory
alkalosis
   pCO2  [HCO3
-]
25

26. ACIDOSIS
 Principal effect of acidosis is depression of the CNS
through ↓ in synaptic transmission.
 Generalized weakness
 Deranged CNS function the greatest threat
 Severe acidosis causes
 Disorientation
 coma
 death
26

27. 27

28. ALKALOSIS
 Alkalosis causes over excitability of the central
and peripheral nervous systems.
 Numbness
 Lightheadedness
 It can cause :
 Nervousness
 muscle spasms or tetany
 Convulsions
 Loss of consciousness
 Death
28

29. 29

30. OUTLINE OF ACID-BASE INTERPRETATION
RULES
Step 1 : Determine if data
is consistent using
Henderson’s Equation
Step 2 : Check pH &
PaCO2 (If either of them
is normal, or both are
normal, got to step 6 to
diagnose mixed acid-
base disorder)
Step 3 : Determine
Primary acid base
disorder
Step 4 : Check for
compensation
Step 5 : Check Anion
Gap/hypoalbuminemia or
delta/delta
Step6 : Mix Acid Base
disorders
30

31. RESPIRATORY ACIDOSIS
31

32. RESPIRATORY ACIDOSIS
 Carbonic acid excess caused by blood levels of
CO2 above 45 mm Hg.
 Hypercapnia – high levels of CO2 in blood
 Chronic conditions:
 Depression of respiratory center in brain that controls
breathing rate – drugs or head trauma
 Paralysis of respiratory or chest muscles
 Emphysema
32

33. RESPIRATORY ACIDOSIS
 Acute conditions:
 Adult Respiratory Distress Syndrome
 Pulmonary edema
 Pneumothorax
33

34. COMPENSATION FOR RESPIRATORY
ACIDOSIS
 Kidneys eliminate hydrogen ion and retain
bicarbonate ion
34

35. ACID–BASE BALANCE DISTURBANCES
Respiratory acidosis.
35

36. RESPIRATORY ALKALOSIS
36

37. RESPIRATORY ALKALOSIS
 Carbonic acid deficit
 pCO2 less than 35 mm Hg (hypocapnea)
 Most common acid-base imbalance
 Primary cause is hyperventilation
37

38. RESPIRATORY ALKALOSIS
 Conditions that stimulate respiratory center:
 Oxygen deficiency at high altitudes
 Pulmonary disease and Congestive heart failure – caused by
hypoxia
 Acute anxiety
 Fever, anemia
 Early salicylate intoxication
 Cirrhosis
 Gram-negative sepsis
38

39. COMPENSATION OF RESPIRATORY
ALKALOSIS
 Kidneys conserve hydrogen ion
 Excrete bicarbonate ion
39

40. ACID–BASE BALANCE DISTURBANCES
Respiratory Alkalosis. 40

41. METABOLIC ACIDOSIS
41

42. METABOLIC ACIDOSIS
 Bicarbonate deficit - blood concentrations of bicarb drop
below 22mEq/L
 Causes:
 Loss of bicarbonate through diarrhea or renal dysfunction
 Accumulation of acids (lactic acid or ketones)
 Failure of kidneys to excrete H+
42

43. COMPENSATION FOR
METABOLIC ACIDOSIS
 Increased ventilation
 Renal excretion of hydrogen ions if possible
 K+ exchanges with excess H+ in ECF
 ( H+ into cells, K+ out of cells)
43

44. ACID–BASE BALANCE DISTURBANCES
.
Responses to Metabolic Acidosis
44

45. METABOLIC ALKALOSIS
45

46. METABOLIC ALKALOSIS
 Bicarbonate excess - concentration in blood is
greater than 26 mEq/L
 Causes:
 Excess vomiting = loss of stomach acid
 Excessive use of alkaline drugs
 Certain diuretics
 Endocrine disorders
 Heavy ingestion of antacids
 Severe dehydration
46

47. COMPENSATION FOR METABOLIC
ALKALOSIS
 Alkalosis most commonly occurs with renal
dysfunction, so can’t count on kidneys
 Respiratory compensation difficult – hypoventilation
limited by hypoxia
47

48. ACID–BASE BALANCE DISTURBANCES
.
Metabolic Alkalosis
48

49. ANION GAP
 This step identifies the type of metabolic acidosis
present, i.e., whether it is secondary to an anion that
creates an AG on electrolyte measurement or not.
 The AG is a diagnostic tool to uncover the actual anions
elevated in the blood but not routinely included in our
measurements under normal conditions.
 It is calculated as follows:
AG = serum sodium − serum chloride − serum bicarbonate.
 A normal anion gap is <12 mmol L−1.
49

50. HYPOALBUMINEMIA
 In this step interpreting metabolic acidosis is
adjusting for factors that would falsely lower the
anion gap if one existed, e.g.,
 hypoalbuminemia and lithium
 or bromide ingestion
 Adjusted AG in hypoalbuminemia = observed AG +
[2.5(normal albumin − observed albumin)].
50

51. DELTA/DELTA
 This step is the comparison of the degree of change
in AG with the change in serum bicarbonate, aiming to
assess the extent of contribution of the AG-producing
process to the actual acidosis. This measurement is
called delta/delta:
 delta/delta= ΔAG/ ΔHCO- =(AG -12) / (24 - HCO3-).
51

52. MNEMONIC VERSION OF EXPECTED COMPENSATORY
RESPONSES TO ACID–BASE DISTURBANCES
52
Assuming a normal ABG of pH 7.4, pCO2 40, HCO3− 24,
and utilizing meq L−1 or mmol L−1 for bicarbonate and
mmHg for pCO2,

53. MIXED ACID BASE DISORDER
 If the Arterial pH is relatively normal and the PCO2
and/or HCO3 are abnormal, one can assume that a
mixed abnormality is present.
53

54. MIXED ACID BASE DISORDER
 Diagnosed by combination of clinical assessment, application of
expected compensatory responses , assessment of the anion gap,
and application of principles of physiology.
 Respiratory acidosis and alkalosis never coexist
 Metabolic disorders can coexist
Eg: lactic acidosis/DKA with vomiting
 Metabolic and respiratory AB disorders can coexist
Eg: salicylate poisoning (met.acidosis + resp.alkalosis) 54

55. 1-CASE STUDY
 11 year old girl
 Mild bronchial asthma with fever and increased
breathing
 Asthmaticus diagnosed
 ABGs Ph 7.22
 p CO2 38mmHg
serum bicarbonate 15med L-1
Serum albumin level 1gdL-1
 What is your interpretation …………….?
 Hypoalbuminemia ( primary metabolic acidosis and
acute respiratory acidosis )
55

56. 2-CASE STUDY
 2 year old child was foun unconscious increased
breathing
 ABGs pH 7.38
pCO2 28mmHg
serum bicarbonate 16 meqL-1
 What is your interpretation……………?
 Salicylate poisoning
56