Maternal physiology: Respiratory
Advanced, Clinical Subspecialties
Progressive increase in ligamentous laxity peaks at 37 weeks due to the hormone relaxin, which increases the AP and transverse diameters of the lower rib cage while decreasing the height of the chest cavity due to elevation of the diaphragm.
As the chest wall expands to a greater resting diameter due to the effect of relaxin, a greater percentage of the work of inspiration is imparted to diaphragmatic excursion.
Items that remain unchanged on PFTs include: the shape of flow-volume loops, FEV1, and FEV1:FVC. Closing capacity also remains unchanged.
Lung volumes and capacities:
Total lung capacity and residual volume are slightly decreased. Overall, the changes in pregnancy are reciprocal as there is a finite total lung capacity. Tidal volume increases by 45% while inspiratory reserve volume decreases; these changes result in increased inspiratory capacity by 15% while expiratory reserve volume decreases. Functional residual capacity steadily decreases during the latter half of pregnancy to 80% of pre-pregnancy volume due to the cephalad movement of the diaphragm; this decrease is made up of decreases to the RV and ERV. The decrease in FRC can be worsened by assuming the supine position, the effect of which can be somewhat ameliorated by increasing the head of the bed by 30 degrees. In the supine position, FRC can be less than closing capacity, resulting in closure of small airways. The FRC remains below pre-pregnancy values for 1-2 weeks after delivery.
In the first trimester, there is an increase in minute ventilation via increased tidal volume and a slight increase in respiratory rate. This effect is prompted by progesterone as well as increased production of CO2. As the amount of dead space remains the same, the overall result is of increased alveolar ventilation by 30-50%. The increase in alveolar ventilation is matched by an increase in cardiac output, resulting in decreased gradient between the end-tidal CO2 and PaCO2. By 72 hours post-partum, the minute ventilation decreases halfway back to pre-pregnancy values, but remains elevated for at least 6-8 weeks. PaO2 increases to 100-105mmHg. Dyspnea is common and is the result of awareness of increased respiratory drive, decreased PaCO2 (~30mmHg by second trimester), enlarging uterus, increased pulmonary blood volume, anemia, and nasal congestion. The decreased PaCO2 is incompletely metabolically compensated as serum bicarbonate ~ 20mEq/L with increase in pH by 0.02 to 0.06.
Changes during labor:
- 1st stage of labor - Minute ventilation increases by 70-140%, oxygen consumption increases by 40% (compared to pre-pregnancy values)
- 2nd stage of labor - Minute ventilation increases by 120-200%, oxygen consumption increases by 75%
- The metabolic demand for oxygen still outstrips supply, as evidenced by an increase in lactate.
Updated definition 2020:
Pregnancy leads to significant alterations in
- Upper airway
- Lung volumes and ventilation
- Oxygen consumption and metabolic rate
Table 1 – summary of changes in various respiratory parameters in a pregnant patient at term as compared to non-pregnant patient
Value near term compared with non-pregnant value
Increase 0-15%Increase 40-45%
Inspiratory reserve volume
Increase 0-5% (initial decrease)
Tidal volumeFirst trimester Term
Increase 20%Increase 40-45% above non pregnant
Expiratory reserve volume
Functional residual capacity
Decrease 20% by term – begins to decline by 5th month of pregnancy.
Total lung capacity
Labor (First stage)
Increase 40% above prelabor value
Labor (second stage)
Increase 75% above prelabor value
Chest wall excursion
Flow volume loop
Changes begin in first trimester
- Capillary engorgement
- Increased tissue friability, effect on estrogen on nasal mucosa may cause rhinitis, epistaxis
- Edema of mucosal lining of the oropharynx, larynx, trachea – more severe in patients with preeclampsia, in URI and after active pushing as a result of associated increased venous pressure
- Increased risk of bleeding during manipulation of upper airway
- Increased risk of difficult mask ventilation and risk of airway obstruction
- Increased risk of difficult laryngoscopy and intubation – weight gain and increase in breast tissue particularly in women of short stature can make insertion of a laryngoscope difficult
- After extubation, airway may be compromised 2/2 edema with risk of airway obstruction in the immediate recovery period
Precautions under anesthesia
- Gentle suction and placement of devices to prevent bleeding
- Avoid nasal instrumentation
- Minimize attempts at laryngoscopy
- Use cuffed tube with smaller diameter – 6.0-7.0
- Optimize position, and back up airway instrumentation should be available before the first attempt – videolaryngoscope
VENTILATION AND OXYGENATION
Increased O2 demand and CO2 production with hormonal changes, lead to increase in MV in first trimester and stays same for the remainder of the pregnancy – increase in TV more than RR. Increase in MV leads to decrease in PaCO2.
Progesterone effects – direct respiratory stimulant, increases chemosensitivity leading to steeper slope and left ward shift of CO2 ventilatory response curve. Occurs early in pregnancy and remains constant till delivery.
However, pH (venous, capillary and arterial) is only mildly alkalotic (7.42-7.44) because of metabolic compensation with increased renal excretion of HCO3 and reduction in serum bicarbonate concentration, the base excess by 2 to 3mEq/L and total buffer base by approximately 5mEq/L. This compensation is incomplete. Decrease in HCO3 affects ability to buffer an acid load. The slight respiratory alkalosis would normally shift the ODC to the left, however a concurrent increase in 2,3 BPG causes the curve to shift to the right.
Ratio of total dead space to tidal volume remains constant during pregnancy, resulting in increase in alveolar ventilation 45% over baseline
Early in gestation, PaO2 on room air, >100 mmHg 2/2 hyperventilation and associated decrease in alveolar CO2. As pregnancy progresses, O2 consumption continues to increase and CO increased to a lesser extent, resulting in reduced mixed venous oxygen content and increased arteriovenous oxygen difference. Later, PaO2 becomes normal or even slightly decreased in supine position, most likely reflecting small airway closure with normal tidal volume ventilation and intra pulmonary shunt. Improves with lateral position – improves arterial oxygenation and reduced A-a oxygen gradient.
Maternal ODC, shifts to right, P50 increases to 30 at term. Higher P50 in the mother and lower P50 in the fetus means that the fetal blood has higher affinity for O2 and offloading of O2 across placenta is facilitated.
Labor and puerperium
Pain of labor, anxiety and coached breathing can lead to severe hyperventilation causing PaCO2 to occasionally decrease below 20mmHg.
MV in unmedicated parturient increases by 70% to 140% in the first stage of labor and by 120% to 200% in the second stage of labor as compared to prepregnancy values.
Oxygen consumption increases above pre labor values by 40% in first stage and 75% in second stage of labor 2/2 increased metabolic demands of hyperventilation, uterine activity and maternal expulsive efforts. Progressive elevation of blood lactate conc as anaerobic metabolism increases. Effective neuraxial analgesia prevents these changes during the first stage of labor and mitigates changes during second stage of labor.
FRC remains below the pre pregnancy volume for 1-2 weeks. Although MV decreases halfway towards non pregnant values by 72 hours, oxygen consumption, tidal volume and MV remain elevated until at least 6 to 8 weeks after delivery. Alveolar and mixed venous PCO2 increase slowly after delivery and are slightly below prepregnancy levels at 6-8 weeks postpartum.
ABG in pregnancy
Blood gas value
PaCO2 declines to 30mm Hg in first trimester and does not change further. Non pregnant patients have a gradient ETCO2 and PaCO2, the two measurements are equivalent during pregnancy and postpartum period as well. This is due to reduction in alveolar dead space which results from increased CO and increased basilar Atelectasis during pregnancy. Mixed venous pCO2 is 6-8mm Hg below non pregnant level from late in first trimester until term.
- Decrease in FRC starts with 5th month of pregnancy– nearly equal reduction in both ERV, RV
- Reduced FRC/CC ratio – more rapid small airway closure with reduced lung volumes, in supine position – FRC can be less than CC for many small airways, giving rise to Atelectasis.
- Increased MV with decreased FRC – more rapid rate at which changes in the alveolar concentration of inhaled anesthetics can be achieved
- During induction of GA – desaturation and subsequent hypoxemia occur more rapidly than in a non-pregnant patient 2/2 decreased O2 reserve (secondary to decreased FRC) combined with increased O2 uptake (2/2 increased metabolic rate).
- Preoxygenation critical for patient safety – 100% for 2-3 minute with goal of end tidal oxygen fraction greater than 0.9, high flow humidified nasal oxygen is not effective in term pregnant women.
- Supine position FRC decreases by 10%, 30 degree head up position can increase FRC by 10%
Dyspnea in pregnancy
- Increased respiratory drive
- Decreased PaCO2
- Increased O2 consumption from enlarging uterus and fetus
- Larger pulmonary blood volume
- Nasal congestion
Begins in first or second trimester, improves as pregnancy continues
Exercise has no effect on pregnancy induced changes in ventilation or alveolar gas exchange
Hypoxic ventilatory response is increased during pregnancy to twice the normal level 2/2 increase in estrogen and progesterone levels. This occurs despite blood and CSF alkalosis.