Respiratory physiology

Ventilation and lung volumes

• Minute ventilation = tidal volume x rate; alveolar ventilation = (tidal volume minus dead space) x rate. With 250 mL breaths at 32/min and 150 mL dead space, alveolar ventilation is only 3.2 L/min: rapid shallow breathing wastes ventilation.
• PaCO2 is proportional to CO2 production divided by alveolar ventilation.
• Alveolar gas equation: PAO2 = FiO2 x (barometric minus water vapour pressure) minus PaCO2/0.8. At sea level in late pregnancy: 0.21 x 713 minus 30/0.8 = about 112 mmHg.

• Lung-protective ventilation: tidal volume 6–8 mL/kg of predicted (ideal) body weight, because lung size follows height and sex, not weight.
• Hypoxic pulmonary vasoconstriction: low alveolar PO2 closes potassium channels in pulmonary arteriolar smooth muscle, depolarising it; blood is diverted from poorly ventilated alveoli. The pulmonary circulation is the one bed where hypoxia constricts rather than dilates.
• Inhaled foreign bodies (a peanut) usually lodge in the right main bronchus, which is wider, shorter and more vertical.

Respiratory changes in pregnancy

• Progesterone acts centrally: the CO2 response curve is shifted to the left with a steeper slope, so ventilation is higher at any PaCO2.
• The diaphragm rises about 4 cm, but its excursion increases; the subcostal angle widens. Chest wall compliance falls; lung compliance is unchanged.
• Lower airway resistance falls because progesterone relaxes bronchial smooth muscle, despite upper airway mucosal swelling. Carboprost (PGF2-alpha) can cause bronchospasm in asthmatics.
• Pulmonary blood flow rises about 45% with unchanged pulmonary artery pressure through recruitment and distension of pulmonary vessels. Women with fixed pulmonary hypertension cannot recruit and decompensate.
• Normal pregnant gas: pH about 7.44, PaCO2 30 mmHg, bicarbonate about 20 mmol/L, PaO2 about 104 mmHg: compensated respiratory alkalosis. A PaCO2 of 40 mmHg in a pregnant asthmatic means dangerous CO2 retention.
• 2,3-DPG rises about 30%: the maternal curve shifts right (P50 rises), so more oxygen is released at the placenta. HbF binds 2,3-DPG poorly, so its curve stays to the left and the two curves move apart.
• Preoxygenation is faster because higher minute ventilation washes out a smaller FRC; but the small FRC and high oxygen use make desaturation during apnoea faster too.
• Labour hyperventilation without analgesia can drive PaCO2 very low. Between contractions PaCO2 sits below the apnoeic threshold, so she stops breathing and desaturates; hypocapnia also constricts uterine vessels. Systemic opioids worsen this.
• Spinal block to T4 weakens cough while the diaphragm (C3–C5) maintains ventilation.

Oxygen carriage

• Content = 1.34 x Hb (g/dL) x SaO2 + 0.003 x PaO2. Delivery = content x cardiac output.
• Worked example: Hb 11, SaO2 98%: 1.34 x 11 x 0.98 = 14.4 mL per dL = 144 mL per litre. Times 6 L/min = about 870 mL/min. Convert to mL per litre before multiplying by output in L/min.
• Landmarks: PaO2 60 mmHg gives about 90% saturation; 40 mmHg about 75%; P50 about 27 mmHg.

• Raised PaCO2 causes respiratory acidosis, a right-shifted curve, cerebral vasodilatation (raised intracranial pressure) and stimulates ventilation through central chemoreceptors.
• Central cyanosis needs about 5 g/dL deoxygenated haemoglobin, so severe anaemia hides it.
• Peripheral chemoreceptors sense PaO2, not content: in anaemia ventilation does not rise. Hyperventilation is driven by low PaO2 or high PaCO2 and acidosis, not by high PO2.

Types of hypoxia

• V/Q mismatch is the commonest cause of hypoxaemia; it corrects well with oxygen.
• Shunt does not correct with 100% oxygen: alveolar PO2 near 670 mmHg with PaO2 only 70 mmHg means blood is bypassing ventilated alveoli (atelectasis, consolidation, right-to-left cardiac shunt).
• Hypoventilation (opioids, residual neuromuscular block after surgery) raises PaCO2 with a normal A–a gradient.
• Anaemic hypoxia: PaO2 and saturation are normal, but content and delivery are low; breathlessness on effort, no cyanosis.
• Cellular hypoxia stops ATP production, so the Na/K-ATPase fails, sodium and water enter, and cells swell; anaerobic glycolysis makes lactate.

Methaemoglobin and carbon monoxide

• Methaemoglobin (iron in the ferric state) follows prilocaine, benzocaine, nitrates or dapsone: slate-grey cyanosis, chocolate blood, oximeter near 85% despite normal PaO2.
• Methylene blue accepts electrons from NADPH-dependent methaemoglobin reductase and becomes leucomethylene blue, which reduces methaemoglobin back to haemoglobin. In G6PD deficiency NADPH is short, so methylene blue fails and may cause haemolysis; give ascorbic acid or exchange transfusion.
• Carbon monoxide: oximeter reads falsely normal. 100% oxygen shortens its half-life from about 4–5 hours to about 1 hour; the fetus clears it more slowly.
• Altitude: hyperventilation first (respiratory alkalosis, then renal bicarbonate loss), later erythropoietin; patchy hypoxic vasoconstriction causes high-altitude pulmonary oedema.

Acid–base and cord gases

• Rebreathing into a paper bag raises PaCO2 and lowers pH back towards normal in hyperventilation. Alkalosis increases calcium binding to albumin, lowering ionised calcium (tingling, carpopedal spasm).

Remember PaCO2 follows CO2 production divided by alveolar ventilation; pregnancy raises the divisor far more.

Exam trap A PaCO2 of 40 mmHg is normal outside pregnancy but signals respiratory failure in a pregnant woman.

Exam trap Hypoxaemia that does not improve on 100% oxygen is shunt; V/Q mismatch improves.

How FCPS asks about this

• Volume in the lungs after a normal tidal expiration: functional residual capacity.
• Pregnant blood gas: compensated respiratory alkalosis, PaCO2 about 30 mmHg, bicarbonate about 20 mmol/L.
• Effect of raised 2,3-DPG in pregnancy: right shift, P50 rises, more oxygen to the fetus.
• Chronic respiratory acidosis: pH near normal, bicarbonate raised.
• Hypoxia that vasoconstricts: pulmonary arterioles (hypoxic pulmonary vasoconstriction).
• PaO2 stays low on 100% oxygen: right-to-left shunt.
• Local anaesthetic causing cyanosis with low saturation: prilocaine, via methaemoglobinaemia; treat with methylene blue.