This chapter is not relevant to any specific Section from the 2017 CICM Primary Syllabus, because there is no specific entry for pregnancy in the Respiratory section. However, the examiner's foreword feels it is Important to note that all trainees are expected to have, "for all sections of the Syllabus an understanding of normal physiology, and physiology [of]...pregnancy" . So, this chapter deals with the respiratory changes which occur during pregnancy. It appears here because the college, in Question 18 from the second paper of 2020 and Question 13 from the first paper of 2012, asked the candidates to "describe the respiratory changes that occur throughout pregnancy". Before the Part One existed, the college had also asked about this in the Fellowship exam, in Question 18 from the first paper of 2006.
Respiratory Changes that Occur in Pregnancy
Pregnancy-related changes Effect of these changes Airway function and structure Mucosal oedema in the upper airway
- Greater resistance to flow
- Bag-valme-mask ventilation becomes more difficult
- Greater risk of airway obstruction with sedation
Structural properties of the chest wall and lung volumes Anatomical changes
- The diaphragm is pushed up by 4cm
- Diaphragmatic excusion increases by about 2cm
- Rib cage expands: subcostal angle of the ribs at the xiphoidal level
increases from 68.5° at the beginning of pregnancy to 103.5° at term
- Anatomical dead space increases by about 445% due to increased airway diameter late in pregnancy
- Tidal volume increases by ~ 30-50%
- Respiratory rate increases to 15-17
- Minute volume increases by 20-50%.
- TLC is reduced by about 5%
- IC is increased by about 10%
- FRC is decreased by about 20%
- Chest wall compliance decreases due to increased fat and abdominal content
- Lung compliance remains the same
- Resistance to air flow in the lower airways increases in early pregnancy, and decreases in late pregnancy
- FEV1/FVC is stable over the course of pregnancy
Gas exchange and gas transport Blood gas tension
- PaCO2 decreases
- PaO2 increases
- Maternal erythrocytes produce higher levels of 2,3-DPG
- p50 remains normal (by the combined effects of 2,3-DPG increase and alkalosis)
Control of ventilation
Central respiratory control
- Progesterone-associated chronic respiratory alkalosis develops (due to increased sensitivity to CO2)
Respiratory workload and demand
Demands on the respiratory system
- Increased body mass (increased weight plus one extra organism on board) = increased total body oxygen demand (by about 21%) and increased ventilatory requirements for the clearance of the excess CO2
- During labour, the oxygen consumption increases by about 60%.
There is a good article by Hegewald & Crapo which summarises the respiratory physiology of pregnancy in clear and concise terms. LoMauro & Aliverti (2015) also have a short review (they described it as a "physiology masterclass") which covers essentially the same ground.
Now, in some detail:
Changes to respiratory anatomy and lung volumes in pregnancy
Overall, this can be summarised as "less FRC and more VT". Realistically, a good author could just leave it there, to respect their reader's time. So, here is a big confusing diagram followed by several hundred words:
- The diaphram is pushed up by 4 cm on average. Weirdly, not all of this is due to to the effect of the gravid uterus pushing up the abdominal contents. Apparently the hormone-induced laxity of rib ligaments begins well before the uterus becomes large enough to shove any abdominal contents into the chest cavity. This, however, does not decrease the mechanical effectiveness of the diaphragm, and if anything it works more efficiently during pregnancy, with an increase in diaphragmatic excursion by about 2cm.
- Tidal volume increases by ~ 30-50%. The increased diaphragmatic excursion changes the tidal volume from (let's say) 500ml in the first trimester to over 700ml in the third trimester.
- Respiratory rate increases from 15 to 17 on average; thus, minute volume increases by 20-50%. This seems to be driven by progesterone, as will be discussed later.
- Chest wall compliance decreases (but lung compliance remains the same). As one might imagine, the workload of the ventilator turbine is somewhat increased by the increased weight of the chest wall, owing particularly to the large turgid breasts heaving around upon it. The changes in ribcage configuration and the upward incursion of the diaphragm also play a role, as the normal "bucket handle" mechanics become disturbed. Lastly, the gravid uterus provides a counterpressure to inspiration, in a manner similar to the distended abdomen of an abdominal compartment syndrome.
- Respiratory resistance changes - initially, it increases in early pregnancy, but as the hormone soup becomes thicker the tracheobronchial tree smooth muscle tends to relax, and resistance decreases (Lomauro & Aliverti, 2015). This also has the effect of increasing the anatomical dead space.
- FEV1/FVC remains essentially the same. Milne (1979) reported on the results from 30 pregnant women who, in spite of the changes in their lung volumes, maintained an essentially unchanged FEV1/FVC ratio - it varied from 84% postpartum to 81.8% at term.
Pregnancy-related changes in gas exchange
PaCO2 decreases, and PaO2 increases in pregnancy. The key feature of gas exchange in pregnancy is the increased metabolic rate of the combined mother/foetus organism, with a resulting increase in the total O2 consumption and CO2 production. This part of the equation makes sense. One would, therefore, expect the mother to develop a persistent hypoxia and mild respiratory acidosis, which would lead to a slight increase in respiratory rate and a raised HCO3-.
However, this is not observed. Instead, expectant mothers blow off vast amounts of CO2 and actually generate a mild respiratory alkalosis, with complete renal compensation and a normal pH- in fact this is a perfect model of an isolated, sustained respiratory alkalosis. This unexpected development is the result of progesterone. Progesterone seems to infiltrate the medullary respiratory control centres, adjusting the homeostatic setpoint for CO2. A brilliant study from 1978 led the way by feeding progesterone supplements to 11 healthy male volunteers, and observing how they hyperventilate. The net effect of this is to increase tidal volume and minute volume to a point beyond any maternofoetal oxygen demands or metabolic excretory requirements.
What is the role of this, one might ask? Surely, this physiological phenomenon must offer an evolutionary advantage beyond the preservation of maternal arterial oxygenation during high-altitude pregnancy. Or at least, there shouldnt be any disadvantage, right? However, early studies observing the effect of maternal hyperventilation have suggested that placental blood flow actually decreases in proportion to a decrease in CO2. Just as one might expect to happen in the dysregulated cerebral vessels of a person with a head injury, the immature foetal cerebral vessels also constrict, with frightening implications. Not only that, but the maternal pH is closely shared by the foetus; respiratory alkalosis would result in an increased affinity of maternal haemoglobin for oxygen, decreasing its availability to the foetus - and the foetal hemoglobin-oxygen affinity would increase, decreasing in its availability to the foetal tissues.
In short, it all seems very counterproductive. A review article by Huch (from 1986) summarises the contemporary findings, and is also at a loss for explanations. However, most of the data collected by this and other reviewers have been from healthy mothers who were compelled to hyperventilate by the experimenters. Obviously, normal pregnant hypocapnia has little effect on foetal cerebral vessels, and does not have any adverse effects on maternofoetal oxygen transport.
One might retreat to the simplicity of basic gas physics, such as Dalton's Law: if there is less CO2 in the alveolus, there is "more room" for O2, and therefore maternal arterial oxygenation increases (presumably to create a greater oxygen gradient driving it by diffusion into the placental vessels). Similarly, the slightly decreased maternal PaCO2 creates a gradient for CO2 removal from the foetus, facilitating its movement across the placenta.
A finding which lends some credibility to this theory is the discovery that maternal erythrocytes produce higher levels of 2,3-DPG during pregnancy, with a resulting decrease in the affinity of maternal hemoglobin for oxygen. One can expect this feature to enhance the delivery of oxygen to the foetus, particularly in the low oxygen tension environment of placental vessels. In the maternal bloodstream, this 2,3-DPG accumulation would produce a right shift of the oxyhemoglobin dissociation curve if there was no alkalosis - but the borderline alkalaemic pH of the late-term gravida (7.40-7.47) pushes the curve in the opposite direction, and the next effect of these competing influences is actually a preserved p50 value.
In summary, over the course of your pregnancy you an expect to develop a progressively lower CO2 and a progressively higher O2. In spite of this, because of several competing influences on the affinity of maternal haemoglobin for oxygen, the effectiveness of maternal oxygen transport seems to be largely unaffected.
A chronology of the respiratory changes in pregnancy
The college, in their comment for Question 18 from the second paper of 2020, remarked that "a straightforward structure including first, second and third trimester delineation would have elevated many answers from below par to a pass." This is not the structure which came to the author intuitively, as the changes of pregnancy are gradual rather than stepwise, and are not discussed in this format in any of the major textbooks. In fact, the act of constructing such a table had taken the author through some hoary backwoods of respiratory physiology, where CICM trainees would not normally tread, so some might argue that this effort would merit something more than just a pass. Specifically, the lung volume data comes from Milne (1979) and the blood gas values come from Hedgewald & Crapo (2011), who only had first and third trimester values listed. From these, the second trimester data were extrapolated for the table in a completely unscientific manner, as a raw mathematical mean.
|Parameters||Not pregnant||First trimester||Second trimster||Third trimester|
|Compliance||Normal||Slight decrease||Moderate decrease||Significant decrease|
|Resistance||Normal||Slight decrease||Moderate decrease||Significant decrease|
|Minute volume||8.5 L/min||10.5 L/min||10.0 L/min||10.5 L/min|
|TLC||5000 ml||5000 ml||4500 ml||5000 ml|
|FRC||2600 ml||2600 ml||2300 ml||2100 ml|
|RV||1300 ml||1300 ml||1100 ml||1000 ml|