Acid base balance full details for md exams 10 marks answer

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ACID-BASE BALANCE - Comprehensive MD Exam Answer (10 Marks)

1. NORMAL ACID-BASE HOMEOSTASIS

Systemic arterial pH is maintained between 7.35 and 7.45 by three integrated mechanisms:

Extracellular and intracellular chemical buffers (immediate, seconds)
Respiratory regulation of PaCO2 (minutes to hours)
Renal regulation of plasma HCO3- (hours to days)

The relationship between these components is expressed by the Henderson-Hasselbalch equation:

pH = pK' + log [HCO3-] / (0.03 x PaCO2)

Where pK' = 6.1, and 0.03 is the solubility coefficient of CO2. At steady state, pH = 7.4 when [HCO3-] = 24 mEq/L and PaCO2 = 40 mmHg.

Normal daily acid production: ~50-70 mEq of fixed (non-volatile) acid from metabolism.

2. BUFFER SYSTEMS

A. Bicarbonate Buffer (most important extracellular buffer)

CO2 + H2O ⇌ H2CO3 ⇌ H+ + HCO3-

pKa = 6.1 (far from physiological pH, yet most effective because CO2 is an open system - lungs continuously regulate CO2)
Buffers ~50% of acid load

B. Proteins (Hemoglobin - most important intracellular buffer)

Hb is the major intracellular buffer in blood
Deoxyhemoglobin is a better buffer than oxyhemoglobin (Haldane effect)

C. Phosphate Buffer

HPO4²- / H2PO4- system (pKa = 6.8)
Important in urine acidification and intracellular buffering

D. Bone Buffer

In chronic acidosis, bone carbonate and phosphate are mobilized - contributes to osteomalacia/osteoporosis

3. RESPIRATORY REGULATION

The respiratory system controls PaCO2 by adjusting alveolar ventilation:

Acidosis → stimulates peripheral (carotid body) and central chemoreceptors → hyperventilation → decreased PaCO2 → pH rises
Alkalosis → decreased chemoreceptor drive → hypoventilation → increased PaCO2 → pH falls

Respiratory compensation is rapid (minutes to hours) but incomplete - it returns pH toward, but not to, normal.

4. RENAL REGULATION

The kidney regulates pH by:

Reabsorption of filtered HCO3- (proximal tubule: 80-85%; TAL and distal: remainder)
Titratable acid excretion (mainly as H2PO4- in distal tubule)
Ammonium (NH4+) excretion - most important for net acid excretion
- Proximal tubule generates NH4+ from glutamine
- NH4+ excreted in urine carries H+ out of the body

Renal compensation is slow (days) but complete (fully restores pH in isolated respiratory disorders).

5. CLASSIFICATION OF ACID-BASE DISORDERS

Disorder	pH	Primary Change	Compensation
Metabolic acidosis	↓	HCO3- ↓	PaCO2 ↓ (hyperventilation)
Metabolic alkalosis	↑	HCO3- ↑	PaCO2 ↑ (hypoventilation)
Respiratory acidosis	↓	PaCO2 ↑	HCO3- ↑ (renal)
Respiratory alkalosis	↑	PaCO2 ↓	HCO3- ↓ (renal)

6. COMPENSATION FORMULAS (Critical for MD Exams)

Disorder	Expected Compensation
Metabolic acidosis	PaCO2 = 1.5 x [HCO3-] + 8 ± 2 (Winter's formula)
Metabolic alkalosis	PaCO2 increases by 0.7 mmHg per 1 mEq/L rise in HCO3-
Acute resp. acidosis	HCO3- increases by 1 mEq/L per 10 mmHg rise in PaCO2
Chronic resp. acidosis	HCO3- increases by 3.5 mEq/L per 10 mmHg rise in PaCO2
Acute resp. alkalosis	HCO3- falls by 2 mEq/L per 10 mmHg fall in PaCO2
Chronic resp. alkalosis	HCO3- falls by 5 mEq/L per 10 mmHg fall in PaCO2 (only disorder where pH fully normalizes)

Harrison's Principles of Internal Medicine 22E, p. 411

7. ACID-BASE NOMOGRAM

The Davenport/acid-base nomogram plots pH vs. HCO3- with PCO2 isobars, showing 95% confidence bands for each simple disorder:

Acid-Base Nomogram showing 90% confidence limits for compensation in all primary acid-base disturbances

Acid-base nomogram (Harrison's Principles of Internal Medicine 22E) - shaded zones represent 95% confidence limits for simple disorders

8. METABOLIC ACIDOSIS

Definition

Primary fall in plasma HCO3- (< 22 mEq/L), with compensatory fall in PaCO2.

Causes - classified by Anion Gap

Anion Gap (AG) = Na+ - (Cl- + HCO3-)

Normal AG = 6-12 mEq/L (average ~10 mEq/L)
Corrected AG: add 2.5 mEq/L per 1 g/dL fall in serum albumin below 4.5 g/dL

High Anion Gap (HAGMA) - mnemonic MUDPILES:

M - Methanol
U - Uraemia (renal failure)
D - DKA (diabetic ketoacidosis)
P - Propylene glycol / Paraldehyde
I - Isoniazid / Iron
L - Lactic acidosis (type A: tissue hypoxia; type B: metformin, liver failure)
E - Ethylene glycol
S - Salicylates

Normal Anion Gap (hyperchloraemic) acidosis - mnemonic HARD-UP:

Diarrhoea (most common - loss of HCO3-)
Renal tubular acidosis (types 1, 2, 4)
Ureterosigmoidostomy
Addison's disease
Post-hypocapnia
Carbonic anhydrase inhibitors (acetazolamide)

Delta Ratio (for HAGMA) = (AG - 12) / (24 - HCO3-)

<0.4: pure normal AG acidosis
0.4-0.8: mixed HAGMA + normal AG acidosis
1-2: pure HAGMA
2: HAGMA + concurrent metabolic alkalosis

Clinical Features

Kussmaul breathing (deep, rapid - compensatory hyperventilation in severe metabolic acidosis)
Decreased cardiac contractility, hypotension
Decreased insulin sensitivity, hyperkalaemia
Confusion, lethargy, coma

Treatment

Treat underlying cause
NaHCO3 rarely needed; use if pH < 7.1 or severe acidaemia with haemodynamic compromise

9. METABOLIC ALKALOSIS

Definition

Primary rise in plasma HCO3- (>26 mEq/L), with compensatory hypoventilation (PaCO2 rises).

Causes

Chloride-responsive (urine Cl- <10 mEq/L):

Vomiting/nasogastric suction (loss of HCl)
Diuretics (thiazides, loop)
Post-hypercapnia
Villous adenoma

Chloride-resistant (urine Cl- >20 mEq/L):

Hyperaldosteronism (primary/secondary)
Cushing's syndrome
Bartter's/Gitelman's syndrome
Severe hypokalaemia

Maintenance factors

Volume depletion → increased aldosterone → renal HCO3- retention
Hypokalaemia → increased renal H+ secretion

Treatment

Chloride-responsive: IV saline (0.9%) + KCl; correct the underlying cause
Chloride-resistant: treat underlying mineralocorticoid excess

10. RESPIRATORY ACIDOSIS

Definition

Primary rise in PaCO2 (>45 mmHg) with compensatory rise in HCO3-.

Causes (hypoventilation)

CNS depression	Opiates, sedatives, anaesthesia, brainstem lesion
Neuromuscular	Myasthenia gravis, GBS, poliomyelitis, MND
Airway obstruction	COPD, severe asthma, foreign body
Chest wall	Kyphoscoliosis, obesity hypoventilation
Parenchymal	End-stage pulmonary fibrosis

Acute vs Chronic

Acute: HCO3- rises by 1 mEq/L per 10 mmHg rise in PaCO2; pH falls markedly
Chronic: HCO3- rises by 3.5 mEq/L per 10 mmHg rise in PaCO2; pH nearly normal

Treatment

Treat the cause
Mechanical ventilation if severe
Oxygen cautiously in COPD (avoid eliminating hypoxic drive)

11. RESPIRATORY ALKALOSIS

Definition

Primary fall in PaCO2 (<35 mmHg) with compensatory fall in HCO3-.

Causes (hyperventilation)

Anxiety, psychogenic
Hypoxaemia (pneumonia, PE, high altitude, severe anaemia)
Sepsis (early) - most common cause of resp. alkalosis in ICU
CNS stimulation (salicylates, fever, head injury)
Pregnancy (progesterone effect)
Liver failure (hepatic encephalopathy)
Iatrogenic (mechanical ventilation)

Compensation

Acute: HCO3- falls 2 mEq/L per 10 mmHg fall in PaCO2
Chronic: HCO3- falls 5 mEq/L per 10 mmHg fall - only disorder where full pH compensation can occur

Clinical Features

Paraesthesias (perioral, fingertips), carpopedal spasm
Lightheadedness, syncope
Decreased ionised calcium (alkalosis increases protein binding of Ca2+)

12. MIXED ACID-BASE DISORDERS

Defined as independently coexisting disorders (not just compensation). Common in critically ill patients.

Metabolic acidosis-alkalosis compensation diagram showing uncompensated and compensated states

Acid-base paths during metabolic acidosis and alkalosis (Ganong's Review of Medical Physiology, 26th Ed.)

Mixed Disorder	pH change	Example
Met. acidosis + Resp. acidosis	Severe ↓↓	Cardiac arrest, severe COPD + DKA
Met. acidosis + Resp. alkalosis	May be near normal	Sepsis + shock, salicylate poisoning
Met. alkalosis + Resp. acidosis	May be near normal	COPD + diuretics/vomiting
Met. acidosis + Met. alkalosis	pH variable	DKA + vomiting

Key: If PaCO2 deviates from the predicted compensation (using Winter's formula or compensation table), a mixed disorder is present.

13. SYSTEMATIC APPROACH TO ABG INTERPRETATION (Step-by-Step)

Check pH - acidaemia (<7.35) or alkalaemia (>7.45)?
Check PaCO2 - elevated, normal, or low?
Check HCO3- - elevated, normal, or low?
Identify the primary disorder - which change (CO2 or HCO3-) explains the pH direction?
Calculate expected compensation - using formulas above
Compare actual vs. expected compensation - deviation = mixed disorder
Calculate Anion Gap - if metabolic acidosis present
Calculate Delta Ratio - if HAGMA present
Correlate with clinical context

14. KEY NORMAL VALUES (Reference)

Parameter	Normal Range
Arterial pH	7.35-7.45
PaCO2	35-45 mmHg
HCO3-	22-26 mEq/L
PaO2	80-100 mmHg
Base excess	-2 to +2 mEq/L
Anion Gap	6-12 mEq/L

15. SPECIAL TOPICS FOR MD EXAMS

Renal Tubular Acidosis (RTA) - Normal AG acidosis

Type	Defect	Urine pH	K+	Cause
Type 1 (Distal)	Failure to acidify urine	>5.5	Low	SLE, Sjogren's, amphotericin
Type 2 (Proximal)	Failure to reabsorb HCO3-	<5.5	Low	Multiple myeloma, Wilson's
Type 4	Aldosterone deficiency/resistance	<5.5	High	DM nephropathy, Addison's

Lactic Acidosis

Type A: Tissue hypoperfusion - shock, cardiac arrest, severe anaemia, CO poisoning
Type B: No obvious hypoperfusion - metformin toxicity, liver failure, thiamine deficiency, malignancy

Salicylate Poisoning - Classic Mixed Disorder

Early: Respiratory alkalosis (direct CNS stimulation)
Late: Metabolic acidosis (HAGMA) + Respiratory alkalosis simultaneously
Classic exam scenario

Sources: Harrison's Principles of Internal Medicine 22E (2025), Ganong's Review of Medical Physiology 26th Ed., Medical Physiology (Boron & Boulpaep)

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