The document discusses arterial blood gas (ABG) interpretation, detailing the maintenance of acid-base balance in the body and the mechanisms of respiratory and renal compensation for acid-base disorders. It covers types of acid-base disturbances, including metabolic and respiratory acidosis and alkalosis, along with case reports illustrating conditions like COPD exacerbation and salicylate poisoning. Essential formulas and clinical implications of interpreting ABG results are provided, emphasizing various causes and compensatory mechanisms associated with each disorder.

1. ABG INTERPRETATION WITH
CASE REPORTS
DR ROSHNARA P P

2. • Acid-base Regulation
• Acid-base disorders
• ABG interpretation
• Case Reports

3. ACID-BASE BALANCE
• The homeostatic maintenance of acids and bases within the
body to achieve a physiological pH of approximately 7.4
• Acidemia : Arterial blood pH <7.35
• Alkalemia : Arterial blood pH >7.45

4. • pH = -log aH+
• pH of Plasma is dependant on 2 Independent variables:
1. PCO2  Lungs : ACID COMPONENT
2. HCO3  Kidneys : BASIC COMPONENT

5. RESPIRATORY MECHANISM

6. RENAL MECHANISM
• Excretion of acid & Conserves HCO3-
Na+-H+ Exchange
• H+ into tubular fluid in exchange for Na+
• K+ competes with H+  Hyperkalemia ass with acidosis & vice-versa
Excretion of H+ as Ammonium ions
Reclamation of Filtered Bicarbonate:
• Carbonic Anhydrase in PCT
• Max Plasma conc = 28mmol/L

7. HENDERSON HESSELBACH
EQUATION
pH = 6.1 + log {cHCO3-/cdCO2}
7.4  6.1 + log {20:1}

8. ACID-BASE DISORDERS
• Metabolic Acidosis  Primary bicarbonate deficit
• Metabolic Alkalosis  Primary bicarbonate excess
• Respiratory Acidosis Primary carbon dioxide excess
• Respiratory Alkalosis  Primary carbon dioxide deficit

9. METABOLIC ACIDOSIS
Causes
•1. Production of organic acids that exceeds the elimination
•2. Reduced excretion of acids
•3. Excessive loss of bicarbonate

10. • Anion Gap
• Na – {Cl + HCO3}  12mmol/L in healthy subjects
• d/t Unmeasured anions (proteins,sulphate,phosphate) present
in plasma
• other retained acids  High anion Gap Acidosis

12. HIGH ANION GAP ACIDOSIS
• Methanol
• Uremia
• Diabetic ketoacidosis
• Paraldehyde
• Iron, Isoniazid, Ischemia
• Lactic acidosis
• Ethylene glycol
• Salicylates

13. NORMAL ANION GAP ACIDOSIS
GI fluid loss
• Severe diarrhoea
• Pancreatitis
Renal tubular acidosis
Proximal (type II) RTA
Distal (type I) RTA
Type IV RTA

14. METABOLIC ALKALOSIS
• Excess base is added to the system
• Base elimination is decreased
• Acid -rich fluids are lost
• Above pH 7.55tetany is a decrease concentration of ionized
calcium due to increase binding of calcium ions by albumin as
H+ ions decrease

15. Cl Responsive Cl Resistant Exogenous Bases
Hypovolemia
Contraction alkalosis
• prolonged vomiting
• nasogastric suction
• Loop diuretics
• Dehydration
• Primary hyper
aldosteronism
• Cushing syndrome
• Bartter syndrome
• Massive blood
transfusion (Sodium
citrate overload)
• Milk Alkali syndrome

16. RESPIRATORY ACIDOSIS
• Factors that directly depress the respiratory centre
Drugs such as narcotics
CNS trauma, tumor, Infections of the CNS
Comatose states
• Conditions that affect the Respiratory apparatus
COPD (most common)
Severe pulmonary fibrosis
Disease of the upper airway
Impaired lung motion due to pleural effusion
ARDS
• Others:
Abdominal distension as in peritontitis and ascites
Extreme obesity
Sleep disorder, sleep apnea

17. RESPIRATORY ALKALOSIS
• Non-pulmonary stimulation of respiratory center
Anxiety, hysteria
Febrile state
Metabolic encephalopathy
CNS infection
Cerebrovascular accident
Hypoxia
Drugs and agents such salicylates, cathecholamines
• Pulmonary disorder
Pneumonia
pulmonary emboli
Interstitial lung disease
CHF
Respiratory compensation after correction of metabolic acidosis
• Others
Ventilation induced hyperventilation

18. HOW TO INTERPRET AN ABG?

19. 1. Acidosis or Alkalosis ?
2. Respiratory or Metabolic?
3. Mixed acid-base disturbance ?
4. Compensation ?
5. Adequate compensation?

21. DEFECT Primary
Change
Compensator
y response
Expected Compensation
Metabolic
Acidosis
HCO3 PCO2 PCO2 falls by 1-1.3mmHg  1mmol/L of
HCO3
{last 2 digits of pH = PCO2}
Metabolic
Alkalosis
HCO3 PCO2 PCO2 inc by 6mmHg  10mmol/L of
HCO3
{HCO3 + 15  last 2 digits of pH}
Acute
Resp Acidosis
PCO2 HCO3 10mmHg of PCO2  1mmol/L of HCO3
Chronic
Resp Acidosis
PCO2 HCO3 10mmHg of PCO2  3.5mmol/L of HCO3
Acute
Resp Alkalosis
PCO2 HCO3 10mmHg of PCO2  2mmol/L of HCO3
Chronic
Resp Alkalosis
PCO2 HCO3 10mmHg of PCO2  5 mmol/L of HCO3

22. • A 70 year old man, Known to suffer from COPD, was admitted
to the hospital with an acute exacerbation of his illness. Arterial
Blood Gas Analysis was carried out on admission (A). In spite of
vigorous physiotherapy and medical treatment his condition
deteriorated (B). He was started on artificial ventilation.
Analysis was repeated after 6hours (C). After 12 hours he had
generalized seizures (D).

23. Arterial Blood A B C D
pH 7.30 7.24 7.40 7.54
pCO2 (mm of
Hg)
71.3 82.5 58.5 42.8
Bicarbonate
(mmol/L)
35 35 34 35
Respirator
y
25 +
(3.5*3)=35.5
Chronic
Repiratory
Acidosis
CRA  inadequate
Renal compensation
Norma
l
Steady
state Renal
compensatio
n
Alkalosis
Normal
Continued
Renal
compensation
due to Chronic
ds.
Alkalosis iCal
decreases

24. • A young woman was admitted to hospital 8 hours after she had
taken an overdose of an unknown pill
• pH  7.53
• PCO2  15 mmHg
• HCO3 10 mmol/L
Alkalosis
Respiratory
History Acute
HCO320mmol/L
Non-Respiratory
Acidosis

25. • Na+  140 mmol/L
• K+  4 mmol/L
• Cl-  113mmol/L
Anion Gap = 21 mmol/L  HIGH ANION GAP
Dx: Mixed Acid-base disturbance
Respiratory alkalosis + High anion gap acidosis
Salicylate Poisoning : Respiratory stimulation  Alkalosis
Salicyclic Acid  High anion Gap