Acid base disorders

1. PRACTICAL APPROACH TO ACIDPRACTICAL APPROACH TO ACID
BASE DISORDERSBASE DISORDERS
Dr. Santosh .M.Narayankar .
Department of General Medicine
N.S.C.B. Medical College, Jabalpur

2. Why acid base disorders important in medicine ?
• Commonly encountered in ICU setup.
• May be life threatening by themselves.
• Appropriate diagnosis and management needs
timely interpretation.
• Physicians must be able to interpret the numbers
rapidly and accurately.

3. IMPORTANCE OF pH
• Precise regulation in narrow range of 7.35 to 7.45
is essential.
• Vital for normal cellular enzymatic reactions and
normal ionic concentration.
• Extreme range is < 7.2 or > 7.55 are potentially life
threatening.
• Alteration in pH may be first marker of underlying
disease.

4. BASIC TERMINOLOGIES USED
pH - free H+
ion concentration
inversely proportional to H+
ion concentration
Acid - substance that can donate H+
ion or release
Base - substance that can accept H+
ion or when
added to solution decreases H+
ion
concentration
Anion - Ion with negative charge
Cation - Ion with positive charge
Acidaemia - acidic blood

5. Acidosis - Abnormal process or disease which
reduces pH due to increased acid or
decreased alkali.
Alkolosis - Abnormal process or disease which
increases pH due to decreased acid or
increased alkali.

6. BASIC PHYSIOLOGY OF ACID – BASE
REGULATION
Acids are produced continuously during normal
body metabolism, about 22,000 Meq/L volatile or
organic acids are produced and about 1 Meq/Kg/day
non-volatile acids are produced.
Despite this pH of extracellular b/w 7.35 to 7.45

7. REGULATION OF ACID BASE
• Mainly done by buffers , kidney and lungs.
• Relation b/w metabolic and respiratory regulations
is explained by Handerson-Hasselbalch equation
[HCO3]
pH = 6.1 + log
0.0301 X [PaCO2]
Kidney
= pK + log
lung

8. BUFFERS
• Chemical substance which releases or accepts H+
ions.
• Provides immediate defence for change in pH.
• Fastest but least buffering capacity.

9. Principle buffers in body fluids
Blood - Bicarbonate
Haemoglobin
Plasma protein
Interstitial fluid - Bicarbonate
Intracellular - Protein
Phosphate
CSF - Bicarbonate
Phosphate
Urine - Bicarbonate
Phosphate

10. RESPIRATORY REGULATION
• Excretes volatile acids (Carbonic acid) as CO2
• Regulates PaCO2
• Normal CO2 production balanced with its
excretion.
• Acts in seconds to minutes
If respiratory regulation fails ?

11. RENAL REGULATION
• Most powerful buffer.
• Acts within hours and peaks by 5- 6 days.
• Maintains by plasma bicarbonate concentration
• Mechanism involves 3 methods
(i) Reabsorption of filtered bicarbonate ions
(ii) Excretion of H+ ions by tubular secretion
(iii) Production of new bicarbonate ions
If renal regulation fails ?

12. PRIMARY ACID BASE DISORDERS
• Defined - based on initial disturbance
• If the initial disturbance affects HCO3
- h
1. Metabolic acidosis (Dec. HCO3
-
)
2. Metabolic alkalosis (Inc. HCO3
-
)
• If the initial disturbance affects PaCO2
3. Respiratory acidosis (Inc. PaCO2)
4. Respiratory alkalosis (Dec. PaCO2)

13. Basic
Disorder
pH H+ Primary
Change
Secondary
Change
Metabolic
acidosis
Low High HCO3
low
PaCO2
Decreased
Metabolic
alkalosis
High Low HCO3 high PaCO2
Increased
Respiratory
acidosis
Low High PaCO2 high HCO3
Increased
Respiratory
alkalosis
High Low PaCO2 low HCO3
Decreased
Characteristics of primary acid-base disorders

14. COMPENSATION IN ACID –BASE DISORDERS
• Body response to neutralized the effect of initial
insult on pH homeostasis.
• Primary metabolic disturbance - compensatory
respiratory response.
• Respiratory disturbance – metabolic
compensatory response.
• Handersn –Hasselbalch’s equation explains the
compensation.

15. SAME DIRECTION RULE
• Compensatory response always occurs in same
direction.
Ex.

16. Disorder Prediction of Compensaton
Metabolic acidosis Paco2= (1.5 XHCO3
-
) + 8 ± 2
or
PaCo2 will > 1.25 mmHg per
mmol/L> in[HCO3
-
]
Metabolic alkalosis Paco2 will > 0,75mmHg per
Mmol/L> in [HCo3
-
]
or
Paco2 will > 6mmHg per 10
mmol/L> in [HCo3
-
_]
Respiratory alkalosis Acute
Chronic
[HCo3_] will > 0.2 mmol/L
Per mmHg >in PaCO2
[HCo3_] will > 04mmol/L
Per mmHg>in Paco2
Respiratory alkalosis Acute
Chronic
[HCo3_] will > 0.1 mmol/L
per mmHg >in PaCO2
[HCo3_] will > 0.4mmol/L
Per mmHg>in Paco2
PREDCITION OF COMPENSATORY RESPONSES

17. WHY TO CHECK COMPENSATION?
• Useful to differentiate simple from mixed.
• Expected changes = actual change than disorder
is simple, if more or less disorder is mixed.
• Follows same direction rule if changes are in
opposite direction think of mix disorder.

18. MIXED ACID BASE DISORDERS
• Independent coexistance of >1 primary acid base
disorder .
• Occur in critically ill patients.
• Most common mixed disorder metabolic +
respiratory acidosis.

19. Common mixed acid base disorders

20. EVALUATION AND INVESTIGATION OF ACID
BASE DISORDER
• History and examination.
• Primary investigations.
• ABG it is mandatory investigation for acid base
disorder diagnosis.

21. ABG WHEN AND WHY?
• There is no single right method for deciding when
to get ABG done.
• Needs to be determined after proper evaluation of
individual patient.

22. WHY ABG SELECTIVELY ?
• Requires arterial puncture
• Painful carries small risk of arterial occlusion
• Expensive
• Should not be used as routine investigation.

23. WHEN ABG NEEDED ?
• Emergency and critically ill patients
• History or serum electrolytes suggestive of acid
base disturbance
• Sick patient with significant respiratory distress

24. HOW TO COLLECT BLOOD FOR ABG ?
Technique for Radial artery puncture ?
1. Perform modified Allen’s test
2. Clean the site (local anesthesia is optional)
3. Use 21 gauge needle with syringe
4. Flush syringe and needle with heparin
5. Palpate artery with one hand and enter skin at 45-
degree angle.
6. Obtain 2-4 ml of blood preferably without
aspiration.
7. After withdrawal of syringe, apply firm pressure at
punctured site.

25. SPECIAL PRECAUTIONS
1. Avoid excess of heparin
2. Air bubble should be tapped and removed from
the syringe
3. If lab. Analysis delay sample should be
refrigerated.

26. INTERPRETATION OF BASIC INVESTIGATION
pH - normal value 7.4 (7.35 to 7.45)
Low pH < 7.35 – acidosis
High pH > 7.45 – alkalosis
Equation which defines relationship b/w H+
,
HCO3 and PaCO2 is -
H+
= 24 X (PaCO2 / HCO3)

27. HCO3 (mEq/L) - normal value 24 (22 – 26)
Low < 22 – Metabolic acidosis (primary)
Res. Alkalosis (secondary)
High > 26 – Metabolic alkalosis (primary)
Res. Acidosis (secondary)
Normal HCO3 does not exclude acid base disorders –

28. PaCO2 (mmHg) - normal value 40 (35 – 45)
High (>45) - Res. Acidosis (Primary)
Metabolic alkalosis (Secondary)
Low (< 35) - Res. Alkalosis (Primary)
Metabolic acidosis (Secondary)

29. ANION GAP
• Represents charge difference b/w unmeasured
anion and cat ions.
• Normal anion gap = 12 ± 2 Meq/L
• Anion gap = Na – (Cl + HCO3)
Important Unmeasured anions Un measured Cat ions
1. Anionic proteins 1. Calcium
2. Phosphate 2. Potassium
3. Sulphate 3. Magnesium
4. Organic acids

30. Importance of anion gap -
• AG in metabolic acidosis – for establishing the
etiological diagnosis.
• AG mixed disorders - if high AG metabolic
acidosis associated with normal HCO3 or AG
excess of HCO3 deficit than think of super
imposed metabolic alkalosis.

31. SERUM POTASSIUM
Normal Value - 3.5 – 5.5 Meq/L
Low - Metabolic & respiratory alkalosis ,
diarrhea, RTA
High - Metabolic acidosis due to renal failure
type 4 RTA , DKA, Res. Acidosis.

32. PULSE OXYMETRY
• Measure O2 saturation of arterial blood
• Normal value - 96 – 100 %
• < 90% S/o marked hypoxia (< 60% PaO2)
• Useful for hypoxia screening
• Tells nothing about PaCO2
• Hypercapnia can occur with 100% O2 saturation.

33. DIAGNOSIS OF ACID BASE DISTURBANCES
BY STEP BY STEP ANALYSIS OF ABG -
1. Is there an acid base disorder ?
2. Is there acidosis or alkalosis ?
3. What is the primary acid base disorder ?
4. Calculate the expected compensation
5. Determine the presence of mixed acid base
disorder.
6. Clinical correlation and to establish etiological
diagnosis

34. CLINICAL DISEASES THAT MAY CAUSE ACID
BASE DISORDERS

35. EXAMPLES OF ACID BASE DISORDERS
CASE - 1
A 15 year old boy is brought from
examination hall in apprehensive state with
complain of tightness of chest pH 7.54, HCO3
21 mEq/L, PaCO2 21 mmHg.

36. CASE - 2
A patient with poorly controlled IDDM
missed his insulin for 3 days.
pH 7.1, HCO3 8 mEq/L, PaCO2 20 mmHg,
Na 140 mEq/L, Cl 106 mEq/L and urinary
ketones +++

37. CASE - 3
A patient with severe diarrhoea,
complains of difficulty in breathing.
pH 7.1, HCO3 14 mEq/L, PaCO2 44 mmHg,
& K 2.0 mEq/L.

38. CASE - 4
ABG of patient with CHF on frusemide is as
follows :
pH 7.48, HCO3 34 mEq/L, PaCO2 48 mmHg.

39. CASE - 5
Following sleeping pills ingestion, patient
presented in drowsy state with sluggish
respiration with respiratory rate 4 /min :
pH 7.1, HCO3 28 mEq/L, PaCO2 80 mmHg,
PaO2 42 mmHg

40. CASE - 6
ABG of patient with shock on ventilatory
support since last 4 hours is
pH 7.48, HCO3 14 mEq/L, PaCO2 22 mmHg

41. CASE - 7
Known case of COPD develops severe
vomiting.
pH 7.4, HCO3 36 mEq/L, PaCO2 60 mmHg

42. CASE - 8
A case of hepatic failure has persistent
vomiting
pH 7.54, HCO3 38 mEq/L, PaCO2 44 mmHg