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The prevalence of obstetric patients in critical care is 1 to 9 in 1000 pregnancies, with a 12% to 20% mortality.1-4 The majority of puerperium cases are related to hemorrhage or hypertension, while the majority of postpartum cases are due to hemorrhage and postsurgical complications.5 Physiologic changes associated with pregnancy affect diagnostics and treatment.


Maternal cardiovascular changes occur in the first trimester, may manifest as early as 5 weeks, peak by the end of the second trimester, plateau up to term, and normalize 2 to 12 weeks postpartum.6 This is primarily mediated by estrogen effecting uterine blood flow and progesterone and prostaglandin E2 causing vasodilation of uteroplacental vessels.1 Cardiac output (CO) increases by 30% to 50% from 8 to 28 weeks.3,6 Central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP) are unchanged secondary to reduced systemic vascular resistance (SVR; 20–30%) and pulmonary vascular resistance (PVR; 20–30%).7 After 24 weeks, supine hypotension syndrome is characterized by hypotension, 5 to 10 mmHg below normal, and bradycardia secondary to decrease in cardiac output from compression of the inferior vena cava (IVC) by the gravid uterus. This can be alleviated by a left lateral tilt positioning.3,6,7 During labor, there is an increase of 10% to 20% in CO due to a return of 300 to 500 mL of blood to the maternal circulation with each uterine contraction.3,7

Prothrombogenic effects include changes with coagulation factors such as increased fibrinogen, factor VII, and factor X and decreased factor XI, factor XIII, and platelets.1 The patient’s ability to tolerate up to 1 liter of blood loss during labor counteracts the effects of physiologic anemia (ie, increased plasma volume by up to 50% by term with a much lower increase in red blood cells) and decrease in colloid oncotic pressure (by 14%).3,6,7 There is an increased lower extremity venous pressure from compression of the uterus on the inferior vena cava, causing varicose veins and hemorrhoids.

Pulmonary changes are progesterone mediated, causing an increase in tidal volume (30–35%), minute ventilation (20–40%), and respiratory alkalosis (Paco2 of 28–32 mmHg) with compensatory renal excretion of bicarbonate (CO2 of 18–21 mEq/L) by term.3,6 The gravid uterus causes a 10% to 25% decrease in functional residual capacity with a 4-cm elevation of diaphragm, and much less decrease in total lung capacity secondary to compensation of the thoracic cage.3,6,7 Chest wall and total respiratory compliance decrease with no effect on total lung compliance.3 Maternal-to-fetal oxygen exchange is enhanced by the ability of the fetus to extract oxygen better at higher hemoglobin (Hgb) concentrations, a higher oxygen saturation of fetal hemoglobin (HgbF) (80–90%) compared to that of HgbA (50–55%) at a Po2 of 30 ...

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