The physiologic changes during pregnancy resulting in increased oxygen demand are present during the first and second trimester and progress to term. Tidal volume, respiratory rate, ventilation perfusion mismatch, and carbon dioxide (CO
2) diffusing capacity all increase in pregnancy. Concomitantly, expiratory reserve volume, residual volume, FRC, total lung capacity, airway resistance, arterial oxygen partial pressure, and arterial CO
2 partial pressure are all reduced.
5 Additionally, oxygen consumption and CO
2 production increase linearly with weight gain.
5 CO
2 and
progesterone increase the sensitivity of the medullary respiratory centers, resulting in increased minute ventilation.
5 These cumulative changes decrease the time to desaturation for the gravid female and induce a respiratory alkalosis.
1,5 The lower esophageal sphincter tone is reduced secondary to progesterone,
1 resulting in increased gastric reflux, delayed gastric emptying, and increased risk for aspiration.
Cardiac output is increased up to 50% during pregnancy, which accelerates the onset of paralysis with nondepolarizing paralytics and may affect the duration of action of other medications used for induction. Aortocaval compression by the gravid uterus can be compounded by “obese supine hypotension syndrome”. By placing the pregnant patient, especially the obese pregnant patient, at increased risk of hypotension, syncope, and reduced uterine blood flow, especially in the supine position.
5 Avoid the supine position and consider lateral uterine displacement in these patients.
3 Monitor for signs of hypovolemia in pregnant patients as hypotension may not be evident until a loss of 25% to 30% of the blood volume has occurred.
9,11 The fetus is at greater risk of complications during maternal hypotension.