Acid base balance full details for md exams 10 marks answer

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acid-base disorders

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acid base disorders evaluation compensation Winter equation professional reference

Acid-Base Balance

Definition

Acid-base balance is the maintenance of arterial blood pH within the normal range of 7.35-7.45. It is essential for normal enzyme activity, protein structure, electrolyte distribution, cardiac function, and CNS function.

Acidemia: arterial pH <7.35
Alkalemia: arterial pH >7.45
Acidosis/alkalosis: processes that respectively lower or raise pH. More than one process may coexist.

Normal values:

Parameter	Normal value
Arterial pH	7.35-7.45
PaCO₂	35-45 mmHg, average 40
HCO₃⁻	22-26 mmol/L, average 24
Base excess	-2 to +2 mmol/L

Henderson-Hasselbalch equation

[ \text{pH} = 6.1 + \log \frac{[HCO_3^-]}{0.03 \times PaCO_2} ]

Thus, pH depends on the ratio of:

Kidney-controlled component: bicarbonate, HCO₃⁻
Lung-controlled component: PaCO₂, representing carbonic acid

Normally, the HCO₃⁻:PaCO₂ ratio is approximately 20:1.
Harrison's Principles of Internal Medicine, 22e, p. 410.

Mechanisms maintaining acid-base balance

1. Chemical buffer systems

These act immediately, within seconds, but do not remove acid from the body.

a) Bicarbonate buffer: major extracellular buffer [ H^+ + HCO_3^- \leftrightarrow H_2CO_3 \leftrightarrow CO_2 + H_2O ]

Hydrogen ions are buffered by bicarbonate; the resulting CO₂ is eliminated by the lungs.

b) Protein buffers

Plasma proteins and hemoglobin bind or release H⁺.
Hemoglobin is an important intracellular buffer in red blood cells.

c) Phosphate buffer [ H_2PO_4^- \leftrightarrow H^+ + HPO_4^{2-} ] Important in intracellular fluid and renal tubular fluid.

d) Bone buffer Bone carbonate and phosphate can buffer chronic acid loads, but prolonged acidosis promotes bone mineral loss.

2. Respiratory regulation

This begins within minutes.

The lungs regulate PaCO₂ by altering alveolar ventilation:

Hypoventilation causes CO₂ retention, raises PaCO₂, and produces respiratory acidosis.
Hyperventilation causes increased CO₂ excretion, lowers PaCO₂, and produces respiratory alkalosis.

In metabolic acidosis, chemoreceptor stimulation produces hyperventilation, often Kussmaul breathing, which lowers PaCO₂ and partly corrects pH.

3. Renal regulation

The kidneys act over hours to days and provide the final, sustained control of acid-base balance.

They maintain pH by:

Reabsorbing filtered bicarbonate, mainly in proximal tubule.
Secreting H⁺ in distal nephron and collecting ducts.
Excreting acid as titratable acid, mainly phosphate.
Producing and excreting ammonium, NH₄⁺, which generates new bicarbonate returned to blood.

During acidosis, the kidney increases H⁺ excretion, NH₄⁺ generation, and HCO₃⁻ reabsorption. During alkalosis, it reduces H⁺ secretion and promotes bicarbonate excretion.

Acid-base disorders

There are four primary disorders:

Disorder	pH	Primary abnormality	Compensation
Metabolic acidosis	↓	↓ HCO₃⁻	↓ PaCO₂ by hyperventilation
Metabolic alkalosis	↑	↑ HCO₃⁻	↑ PaCO₂ by hypoventilation
Respiratory acidosis	↓	↑ PaCO₂	↑ HCO₃⁻ by renal retention
Respiratory alkalosis	↑	↓ PaCO₂	↓ HCO₃⁻ by renal excretion

Compensation never overshoots the pH to produce alkalemia in acidosis or acidemia in alkalosis. If it does, a mixed disorder is likely.

1. Metabolic acidosis

Definition

Primary reduction in plasma bicarbonate, causing low pH.

Causes

A. High anion gap metabolic acidosis Occurs from accumulation of unmeasured acids.

Common causes:

Lactic acidosis: shock, sepsis, hypoxia
Ketoacidosis: diabetic, alcoholic, starvation
Renal failure/uremia
Toxins: methanol, ethylene glycol, salicylates, propylene glycol
Advanced chronic kidney disease

B. Normal anion gap metabolic acidosis Also called hyperchloremic metabolic acidosis.

Causes:

Diarrhea or intestinal/pancreatic bicarbonate loss
Renal tubular acidosis
Acetazolamide/carbonic anhydrase inhibitors
Excess 0.9% saline infusion
Ureterosigmoidostomy
Early renal failure

Compensation

Respiratory compensation is hyperventilation.

Winter's formula: [ Expected\ PaCO_2 = 1.5 \times HCO_3^- + 8 \pm 2 ]

Actual PaCO₂ above expected: associated respiratory acidosis
Actual PaCO₂ below expected: associated respiratory alkalosis

Anion gap

[ AG = Na^+ - (Cl^- + HCO_3^-) ]

Normal AG is approximately 8-12 mmol/L without potassium.

Correct for albumin: [ Corrected\ AG = measured\ AG + 2.5 \times (4 - albumin\ in\ g/dL) ]

A raised anion gap nearly always indicates an added metabolic acidosis. Merck's acid-base guide

2. Metabolic alkalosis

Definition

Primary increase in HCO₃⁻ causing alkalemia.

Causes

Chloride-responsive, usually urine chloride <20 mmol/L

Vomiting or nasogastric suction
Loop and thiazide diuretics
Volume depletion
Post-hypercapnic state

Chloride-resistant, usually urine chloride >20 mmol/L

Mineralocorticoid excess: primary hyperaldosteronism, Cushing syndrome
Severe potassium depletion
Bartter or Gitelman syndrome
Excess alkali intake in renal impairment

Compensation

Hypoventilation raises PaCO₂.

[ Expected\ PaCO_2 \approx 40 + 0.7 \times (HCO_3^- - 24) \pm 5 ]

Respiratory compensation is limited because marked hypoventilation would produce hypoxemia.

3. Respiratory acidosis

Definition

Primary elevation of PaCO₂ due to alveolar hypoventilation.

Causes

COPD and severe asthma
Airway obstruction
Severe pneumonia, pulmonary edema, or respiratory muscle fatigue
CNS depression: opioids, sedatives, anesthetics, head injury
Neuromuscular disease: Guillain-Barré syndrome, myasthenia gravis
Obesity hypoventilation syndrome
Chest wall disorders

Renal compensation

Type	Expected HCO₃⁻ change
Acute respiratory acidosis	HCO₃⁻ rises by 1 mmol/L for each 10 mmHg rise in PaCO₂
Chronic respiratory acidosis	HCO₃⁻ rises by 3.5-4 mmol/L for each 10 mmHg rise in PaCO₂

Chronic respiratory acidosis occurs in chronic CO₂ retainers such as COPD. Renal compensation takes about 3-5 days.

4. Respiratory alkalosis

Definition

Primary fall in PaCO₂ due to hyperventilation.

Causes

Anxiety, pain, fever
Hypoxemia: pulmonary embolism, pneumonia, high altitude
Sepsis
Pregnancy
Liver failure
CNS disorders
Mechanical overventilation
Early salicylate poisoning

Renal compensation

Type	Expected HCO₃⁻ change
Acute respiratory alkalosis	HCO₃⁻ falls by 2 mmol/L for each 10 mmHg fall in PaCO₂
Chronic respiratory alkalosis	HCO₃⁻ falls by 4-5 mmol/L for each 10 mmHg fall in PaCO₂

Systematic interpretation of arterial blood gas

Assess pH
- <7.35: acidemia
- 7.45: alkalemia
Identify the primary process
- Low HCO₃⁻ suggests metabolic acidosis.
- High HCO₃⁻ suggests metabolic alkalosis.
- High PaCO₂ suggests respiratory acidosis.
- Low PaCO₂ suggests respiratory alkalosis.
Check expected compensation
- Use Winter's formula in metabolic acidosis.
- Use acute/chronic compensation rules for respiratory disorders.
- Inappropriate compensation indicates a mixed disorder.
Calculate anion gap in metabolic acidosis [ AG = Na^+ - (Cl^- + HCO_3^-) ]
Look for mixed acid-base disorders Suspect these when compensation is outside the predicted range, when pH appears normal despite abnormal PaCO₂ and HCO₃⁻, or when clinical context suggests more than one abnormality.

Clinical importance and management principles

Severe acid-base disturbances can cause arrhythmias, impaired cardiac contractility, hypotension, altered sensorium, seizures, coma, and respiratory failure.

Management is directed at the underlying cause:

Lactic acidosis: restore perfusion and treat sepsis/hypoxia.
Diabetic ketoacidosis: fluids, insulin, potassium replacement.
Diarrheal acidosis: volume, electrolyte, and bicarbonate replacement where indicated.
Metabolic alkalosis due to vomiting/diuretics: isotonic saline and potassium chloride, if chloride-responsive.
Respiratory acidosis: improve ventilation and reverse airway, pulmonary, or CNS cause.
Respiratory alkalosis: correct hypoxemia, pain, sepsis, pulmonary embolism, or ventilator settings.

Sodium bicarbonate is not routine for all metabolic acidosis. It may be considered in selected severe acidemia, especially with very low pH, while definitive therapy treats the cause.

Conclusion: Acid-base balance is maintained by buffers, lungs, and kidneys. ABG interpretation requires identification of pH status, primary disorder, expected compensation, anion gap, and possible mixed acid-base disturbance.

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