Both the anteroposterior and the transverse diameters of the chest increase in pregnancy, and the diaphragm moves upward by about 4 cm [1]. Enlargement of the breasts may affect chest compliance and the ease of intubation [2]. The increase in blood and interstitial fluid volume is responsible for the development of mucosal edema especially in the oropharyngeal and laryngeal structures reducing the airway diameter. Hyperemia, which is possibly related to hormonal changes and the increase in plasma volume, makes the mucosa friable and prone to bleeding with minimal trauma. This increased friability may then compromise the visualization of the upper airway landmarks. Longitudinal upper airway assessment with Mallampati grading system suggests that airways become less patent with pregnancy progression (Pilkington). In addition, Mallampati grades I–II may progress to III–IV during labor and do not return to pre-labor grades for an additional 12 h [2].

During pregnancy, oxygen consumption is increased by 30–60 % [2]. There is a 20 % decline in functional residual capacity by term. An additional drop of nearly 25 % may be observed in the supine position [2]. The increase in oxygen consumption and the reduction in functional residual capacity in the supine position contribute to decreased oxygen reserve and lead to faster desaturations in response to apnea. A study by Choi et al. has shown that compared to nonpregnant controls and following sedation and the use of paralytics, pregnant women have a significantly faster decline in oxygenation and increase in PaCO2 in response to induced apneas [3]. Thus, intubation protocols should be modified in pregnant women to account for these changes.

Pregnancy is associated with profound hemodynamic changes that prepare gravidas for the blood loss that is anticipated during delivery. Blood volume increases by 40–52 % by the end of gestation [4, 5]. This increase begins as early as 6 weeks gestation, peaks in the late second trimester, and then plateaus. Blood volume in pregnancy varies but is generally 1,200–1,600 ml greater than in a nonpregnant individual [6]. The rise in blood volume results from an expansion of erythrocytes as well as significant rise in plasma volume. The latter is due to an increase in sodium and water retention related to enhanced renin-angiotensin-aldosterone system activity, and an increase in the hepatic production of renin related to the hyperestrogenic state of pregnancy [1]. The disproportionate increase in red blood cells to plasma volume results in a physiologic anemia of pregnancy [7].

Heart rate increases by 10–20 % during gestation, but this increase usually occurs in the latter part of pregnancy. Cardiac output (CO) starts rising in the first trimester, peaking by the end of the second trimester [8, 9], and may be as high as 50 % above prepregnancy values. This rise is more pronounced in twin, compared to singleton pregnancies. The rise in CO is caused by a significant increase in preload and stroke volume in the early part of gestation. CO is then maintained in the second half of pregnancy primarily by an increase in heart rate. Nearly 17 % of cardiac output is directed to the uterine arteries to supply a flow of 500 ml/min to the placenta and the growing fetus. Both central venous and pulmonary capillary wedge pressure are unchanged in pregnancy.

Systemic vascular resistance falls early in pregnancy as a result of vasodilation in response to hormonal stimulation [10]. Despite an increase in cardiac output, the end result is a fall in blood pressure (BP) in the first trimester. Diastolic blood pressure falls are more pronounced than systolic blood pressure changes and result in a widened pulse pressure. Mean BP decreases by 10–15 mm Hg starting in the first trimester with a nadir in BP occurring at approximately 24–28 weeks [11]. Similar changes occur in the pulmonary circulation, leading to unchanged pulmonary pressures despite the increase in cardiac output.

Plasma colloid osmotic pressure (COP) falls during normal pregnancy from 23.2 mm Hg in the first trimester to 21.1 mmHg at term [12] to 16 mm after delivery and that fall is even more pronounced in PEC [13]. This drop in colloid osmotic pressure not only contributes to the development of pulmonary edema even in the absence of elevated hydrostatic pressures but also contributes to its higher incidence in the postpartum, compared to the antenatal period.

Aortocaval compression caused by the gravid uterus in the supine position may result in decreased venous return, reduced filling of the right heart cavities resulting in maternal hypotension and potential for uteroplacental insufficiency in women with tenuous intravascular status [2]. Combining these changes with the increased oxygen consumption observed in pregnancy and labor and delivery, the decrease in FRC in the supine position and limited oxygen reserve and the reduction in cardiac output in the supine position may all compromise placental perfusion in susceptible individuals [1].

Gastrointestinal physiologic changes occurring in pregnancy and around labor and delivery complicate airway intubation further. A generalized slowing of the gastrointestinal tract function occurs in pregnancy due to the effect of progesterone on smooth muscles. Lower esophageal sphincter tone is reduced with a subsequent increase of acid reflux frequency [14]. During labor, gastric emptying is slower [2]. The gravid uterus compresses the duodenum and the stomach increasing the chances of regurgitation. When opioids are administered during labor or added to the epidural analgesia, gastric emptying is further delayed, but the use of local anesthetics in epidural analgesia alone has no effect [2].

Obesity is a major issue in the modern world and has reached heights of an epidemic in certain developed countries. Despite efforts to reduce obesity, women of reproductive age and pregnant women are no exception [1]. Obesity is associated with numerous pregnancy-related complications, including anesthesia-related complications. Obesity is a risk factor for difficult intubation in the general as well as in obstetric population: a BMI > 26 kg/m² is by itself a risk factor for difficult mask ventilation [1]. Morbidly obese parturients have a higher incidence of cesarean delivery necessitating anesthetic intervention [2].

Preeclamptic parturients have narrowed upper airways secondary to soft tissue swelling. This is well observed in sitting and supine position [15, 16]. Neck, facial, and tongue edema may be cues for possible difficult airway. Moreover, thrombocytopenia in the settings of preeclampsia constitutes a major risk since it shifts the choice from regional to general anesthesia in the case of an operative delivery. In addition, the risk of bleeding during airway intubation is higher with thrombocytopenia which may significantly impact visualization of the upper airway landmarks and complicate airway intubation further.

Not surprisingly, pregnant women have been excluded from many critical care trials. Hence, many of the data are based on either pregnancy-specific disorders or on expert opinion and logical decisions informed by pregnancy physiology. Indications for hemodynamic monitoring in obstetrics are similar to the non-obstetric population but also include some pregnancy-specific disorders such as severe preeclampsia with refractory hypertension or severe cardiovascular collapse such as in the setting of an acute amniotic fluid embolism. Other indications in obstetrics include structural heart disease with a potential for decompensation during labor and delivery. Indications for hemodynamic monitoring in adult respiratory distress syndrome (ARDS) or septic shock are unchanged in pregnancy compared to the nonpregnant population. In general, conditions requiring hemodynamic monitoring in pregnancy are uncommon. However, when they do occur, interpretation of hemodynamic data requires a good understanding of the physiologic changes associated with pregnancy.

Echocardiography and urinary diagnostic indices are noninvasive monitoring methods that have been evaluated in obstetric patients in small studies. A high correlation between echocardiography and invasive techniques has been seen in the measurement of cardiac output [18, 19], stroke volume, ventricular filling pressure, and pulmonary artery pressures [18] in obstetric patients. In a study of 14 obstetric patients with refractory hypertension and oliguria, the authors reported that 12 of the reported cases were successfully managed without the need for invasive monitoring suggesting that echocardiography may be an effective alternative to pulmonary artery catheterization in pregnancy [20]. In a study evaluating seven oliguric preeclamptic patients [21], urinary indices of volume status including fractional excretion of sodium and urine sodium were inconsistent with findings on pulmonary catheterization. These data suggest that urinary indices alone may be misleading in guiding fluid management in preeclamptic patients. Given the increased hydrostatic pressure, lowered oncotic pressure, and capillary leak associated with preeclampsia, these patients are at very high risk for pulmonary edema.