Effect of Pregnancy on the Respiratory System

Introduction

1. Anatomical Changes

• The enlarging uterus displaces the diaphragm upward by approximately 4-5 cm
• The subcostal angle widens from 68 degrees to 103 degrees - this occurs early in pregnancy even before significant uterine enlargement, suggesting hormonal (relaxin) mediation
• The transverse diameter of the chest increases by approximately 2 cm
• Chest circumference increases by up to 5-7 cm
• Despite the upward displacement of the diaphragm at rest, diaphragmatic excursion during breathing is actually increased by ~1.5 cm

• Mucosal hyperaemia and oedema of the nasal passages, oropharynx, and larynx occur due to oestrogen-mediated increased vascularity
• This produces nasal stuffiness ("rhinitis of pregnancy") and can cause difficult intubation
• Airway resistance actually decreases by ~35% due to progesterone-mediated smooth muscle relaxation

2. Lung Volumes and Capacities

• FRC decreases because both ERV and RV decrease - this is primarily due to upward displacement of the diaphragm
• Vital capacity is preserved despite the mechanical changes, because the increase in IC compensates for the decrease in ERV
• TLC decreases only slightly (-4%)
• The decrease in FRC is clinically important - it reduces the oxygen reserve and predisposes to rapid desaturation during apnoea (e.g., during intubation)

3. Ventilation Changes

• Tidal volume increases by 40-50% (from ~500 mL to ~700 mL)
• Respiratory rate remains unchanged early in pregnancy; rises by only ~10% late in pregnancy
• The result is a 50% increase in minute ventilation (from ~7.5 L/min to ~10.5 L/min)

• Increases by approximately 60 mL in pregnancy, likely due to dilation of small airways

• The primary driver is progesterone, which acts as a direct respiratory stimulant on the central respiratory centre
• Progesterone lowers the CO2 threshold of the respiratory centre and increases sensitivity to CO2: a rise of 1 mmHg in PaCO2 increases ventilation by 6 L/min in pregnancy vs. 1.5 L/min in the non-pregnant state
• An increase in basal metabolic rate also contributes
• Progesterone may also increase red blood cell carbonic anhydrase B levels, facilitating CO2 transfer independently of ventilation changes
• This hyperventilation begins as early as the first trimester

4. Gas Exchange Changes

• Increased minute ventilation causes a compensated respiratory alkalosis
• PaCO2 falls to 28-32 mmHg
• The kidneys compensate by excreting bicarbonate, reducing serum HCO3- to 18-22 mEq/L
• Arterial pH is mildly alkalotic at 7.44 (vs. 7.40 non-pregnant)
• This is a normal finding in pregnancy and should not be labelled pathological

• Respiratory alkalosis shifts the curve to the left - increases maternal Hb affinity for O2 (Bohr effect) - potentially reducing O2 release to the fetus
• This is compensated by an alkalosis-induced increase in 2,3-DPG in maternal erythrocytes, which shifts the curve back to the right, facilitating O2 transfer to the fetus
• Net result: efficient oxygen delivery to the fetus is maintained

5. Oxygen Consumption

• O2 consumption increases by 20-50% by term
• Due to: increased maternal metabolic demands + fetal requirements + increased cardiac work
• Oxygen delivery = Cardiac Output x Arterial Oxygen Content
• Despite the increased O2 demand, the hyperventilation of pregnancy increases PaO2 to 101-104 mmHg, maintaining adequate oxygen delivery
• At higher altitudes, even greater compensatory hyperventilation occurs

6. Airway Changes (Clinically Important)

• Mucosal oedema and capillary engorgement of the upper airway (due to oestrogen)
• Increased risk of nosebleeds (epistaxis)
• Nasal stuffiness throughout pregnancy
• In the third trimester, laryngeal oedema may make intubation more difficult - always use a smaller endotracheal tube (6.0-6.5 mm ID instead of standard 7.5-8.0 mm)
• These changes are exacerbated by pre-eclampsia

7. Dyspnoea of Pregnancy

• Up to 75% of pregnant women experience dyspnoea, usually beginning in the first or second trimester
• Paradoxically, dyspnoea appears before the mechanical effects of the uterus are significant, suggesting a neurochemical mechanism
• It may be due to heightened awareness of the increased ventilatory drive from progesterone
• FEV1 and FVC are unchanged - so spirometry is normal
• Dyspnoea that is severe, progressive, or associated with other symptoms warrants further evaluation

8. Summary Table of Respiratory Changes

9. Clinical Relevance (for MD Exams)

1. Rapid desaturation during apnoea - reduced FRC = decreased O2 reserve. Always pre-oxygenate pregnant patients before intubation.
2. Normal ABG in pregnancy = respiratory alkalosis. A "normal" PaCO2 of 40 mmHg = CO2 retention in pregnant patients.
3. Difficult airway - mucosal oedema, increased Mallampati score, must plan for difficult intubation.
4. Asthma management - pregnancy-induced hyperventilation means the expected PCO2 is lower; a rising PCO2 toward 40 mmHg in an asthmatic pregnant woman signals fatigue and impending respiratory failure.
5. Spirometry is unaffected - FEV1 and FVC remain normal; useful for evaluating true airway disease in pregnancy.

• Creasy & Resnik's Maternal-Fetal Medicine: Principles and Practice
• Morgan and Mikhail's Clinical Anesthesiology, 7e
• Murray & Nadel's Textbook of Respiratory Medicine