Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_540_Библиотеки_им_академика_М_И_Перельмана

Maternal VO2 increases by 15–20% [13]. The resulting respiratory alkalosis is renally compen­sated with increased ventilation by reducing serum bicarbonate to 20mEq/L and total buffer base capacity to 5mEq/L [11]. Thus, the parturi­ent is more vulnerable to hypoxemia and acide­mia when critically ill, with less physiologic reserve than nonpregnant [13]. Also, a 50% increase in plasma volume results in dilutional anemia and an overall rise in circulating blood volume of 40% [11, 13]. Cardiac output increases by 30–50%; blood ow to the gravid uterus increased tenfold [13]. After 20weeks of gesta­tion, the uterus size can cause a mechanical aor­tocaval obstruction while fully supine. The ‘supine-hypotensive syndrome’ result is a signi­cant loss of venous return for which the cardio­vascular system cannot compensate [11]. However, most women develop collateral circu­lation through interosseous vertebral, paraverte­bral, epidural, and ovarian venous systems, less impacted by increased IAP [11]. Those suffering from supine-hypotensive syndrome likely do not develop adequate collateral circulation [14]. While only approximately 8% of women at term experience this life-threatening situation, signi­cant compression of the inferior vena cava while supine occurs in most women [11, 14]. Whether elevated IAP can exacerbate aortocaval compres­sion and has a relationship with this syndrome is unknown. Thus, due to the myriad of hormonal, mechano-physiologic changes, the majority of parturients are well compensated for the expo­nential growth of their fetus in a relatively short duration of time.