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Pregnancy and Critical Care Medicine Part 1: Normal Physiologic Changes in Pregnancy
By Andrew M. Luks, MD, Pulmonary and Critical Care Medicine, University of Washington, Seattle, is Associate Editor for Critical Care Alert.
Dr. Luks reports no financial relationship to this field of study.
The overwhelming majority of women who go through pregnancy never require admission to the intensive care unit.1 There are circumstances, however, when these women do require the services of critical care practitioners because they develop respiratory failure, sepsis, or another pregnancy-related complication, or because they have an underlying medical condition, such as pulmonary hypertension, which requires a higher level of monitoring in the peripartum period. Such patients often pose great challenges for critical care practitioners. Due to the relatively low frequency with which they end up in the ICU, familiarity with the underlying physiology of pregnancy and the types of problems that can occur is lower than for other more common problems such as COPD exacerbations or septic shock. In addition, the fact that pregnant women have the potential for rapid clinical decline that puts them, as well as the fetus, at risk for bad outcomes creates an added level of stress that is not present in the care of many other patients.
This special feature is the first of a two-part series designed to reinforce knowledge about the underlying physiology of pregnancy and the major forms of critical illness that may be encountered in these patients. The important physiologic changes will be considered in detail in this issue, while respiratory failure and other forms of critical illness in pregnancy will be dealt with in a subsequent issue of the newsletter. This review will draw on information provided in several general reviews on these topics,2-5 and will cite these reviews rather than the large body of primary literature on these issues. The reader is encouraged to seek out these reviews and, in particular, the excellent, thorough review by Lapinksy and colleagues,2 for more detailed information on these issues.
"Normal" Physiology in the Pregnant Patient
Any critical care practitioner evaluating or managing a pregnant patient must understand the physiologic changes that occur across multiple organ systems over the course of pregnancy. Failure to do so can cause misinterpretation of clinical and laboratory data and lead to inappropriate management steps.
Significant changes occur in the circulatory system during pregnancy. Perhaps the most important of these is a nearly 40% increase in cardiac output and circulating blood volume.2 These changes, which start in the first trimester and peak in the third trimester, are generally well tolerated by most pregnant women, but can cause significant problems for those patients with stenotic valvular lesions or pulmonary hypertension (both known or previously unrecognized). Cardiac output increases even further during labor and delivery, when uterine contractions augment preload by as much as 300-500 mL, as well as immediately following delivery when "auto-transfusion" of uterine blood and release of vena caval compression lead to a significant increase in venous return.2
It is also important to remember that a substantial proportion of the increased cardiac output (~10%, or 500 mL/min) is being delivered to the gravid or postpartum uterus.2 As a result, any patients who experience uterine rupture, uterine atony, or retained placental fragments will be at risk for significant blood loss and hemodynamic instability. It also should be remembered that plasma volume and cardiac output will remain elevated for up to a few weeks following delivery as the patient mobilizes large amounts of extravascular fluid that accumulated over the course of pregnancy.
Uterine enlargement may have significant cardiovascular effects in the latter half of pregnancy. With placement in the supine position, the enlarged uterus compresses the inferior vena cava and significantly decreases venous return and, as a result, cardiac output.3 This phenomenon, referred to as the "supine hypotension syndrome" can be prevented by placing the patients in a lateral position with wedges or pillows under their buttocks and should always be considered during resuscitation of the pregnant patient with hemodynamic instability.3
Despite the increase in cardiac output noted above, systemic blood pressure usually decreases during pregnancy due to a fall in systemic vascular resistance. Both systolic and diastolic blood pressure fall, with greater decreases seen in the latter and a subsequent increase in pulse pressure.2,3 Systemic pressure will rise in the latter part of pregnancy, but should remain below pre-pregnancy values. As a result, the presence of a "normal" or mildly elevated blood pressure should alert the clinician to the possibility of pregnancy-induced hypertension and preeclampsia.
Colloid osmotic pressure is decreased in pregnancy, partly due to the decrease in serum albumin concentrations stemming from the expansion in plasma volume.3 This change puts pregnant women at risk for third-spacing of fluid, volume overload, and pulmonary edema in pathologic processes such as preeclampsia.
While the use of pulmonary artery catheters has declined in recent years following studies questioning their effect on patient outcomes, the complex physiology in pregnant women occasionally may warrant their use for hemodynamic monitoring. As with some common laboratory values referenced in this review, "normal" values for many of the parameters measured with the PA catheter may vary relative to the non-pregnant state and familiarity with these changes can prevent inappropriate management steps. The expected changes in these parameters are described in Table 1 (below).2,3
|Table 1. Changes in hemodynamic parameters in the third trimester of pregnancy.|
|Parameter||Mean Value||Change Compared to Non-pregnant Woman|
|Central venous pressure (mm Hg)||4 ± 2.5||None|
|Pulmonary capillary wedge pressure (mm Hg)||7.5 ± 2||None|
|Cardiac output (L/min)||6.2 ±1||Increased 30%-50%|
|Systemic vascular resistance (dynecmsec-5)||1200 ± 600||Decreased 20%-30%|
|Pulmonary vascular resistance (dynecmsec-5)||75 ± 22||Decreased 20%-30%|
|Adapted from: Lapinsky SE, et al. Critical care in the pregnant patient. Am J Respir Crit Care Med 1995;152:427-455.|
Like the cardiovascular system, the respiratory system undergoes a large number of changes in pregnant women. Minute ventilation increases throughout pregnancy, reaching levels 30%-50% greater than the non-pregnancy baseline by the third trimester.3,5 This is due to both an increase in carbon dioxide production as well as increased levels of progesterone, which acts as both a direct stimulant to minute ventilation and alters sensitivity to carbon dioxide in respiratory centers.2 Because the increase in minute ventilation is out of proportion to the increase in alveolar ventilation requirements, pregnant women typically manifest a compensated respiratory alkalosis, with PaCO2 values around 28-30 mm Hg, bicarbonate values of 18-21 mEq/L, and pH between 7.40 and 7.48. These values are important to remember, as they will affect blood gas interpretation in these patients. More importantly, pregnant women who develop respiratory failure and require mechanical ventilation should be ventilated to this target PaCO2 to avoid alterations in uterine blood flow and fetal oxygen delivery.
The majority of pregnant women are able to meet these minute ventilation requirements as many markers of pulmonary function including diaphragm function, lung compliance, and spirometry are unchanged during pregnancy, although respiratory system compliance does fall in the latter stages of pregnancy due to enlargement of the parturient abdomen and increased weight of the chest wall (see Table 2, below).5 Importantly, however, functional residual capacity (FRC) is decreased 10%-25% as term approaches.3,5 This is generally not an issue for otherwise healthy pregnant women, but can cause significant risks for those who hypoventilate or develop hypoxemic respiratory failure and require intubation and mechanical ventilation. In combination with the 20%-30% increase in oxygen consumption stemming from oxygen utilization by the fetus and increased maternal metabolic activity, the decrease in FRC predisposes pregnant women to rapid onset of hypoxemia, particularly when placed in the supine position. Whereas a well pre-oxygenated 70 kg adult may maintain a stable saturation for up to 7-8 minutes following cessation of ventilation, a pregnant woman may start to desaturate in as little as 1-2 minutes.2,6 Apart from periods of hypoventilation or apnea during intubation attempts, pregnant women typically maintain stable oxygenation and have normal alveolar-arterial oxygen differences when in the upright position.
Table 2. Changes in commonly measured pulmonary function parameters during pregnancy.
|Forced vital capacity||No change|
|Forced expiratory volume in one second (FEV1)||No change|
|Total lung capacity||No change to small decrease (~5%) in late pregnancy|
|Peak expiratory flow rate||No change|
|Diffusion capacity for carbon monoxide||No change|
|Functional residual capacity||Decrease 10%-25%|
|Source: Bobrowski RA. Pulmonary physiology in pregnancy. Clin Obstet Gynecol 2010;53:285-300.|
Pulmonary vascular resistance decreases by 20%-30% in the third trimester2 as a result of recruitment and distention of the pulmonary vasculature in response to the increase in cardiac output and pulmonary blood flow. This will significantly limit the rise in pulmonary artery pressure that would otherwise occur with the rise in cardiac output and helps preserve right heart function. Patients with pulmonary arterial hypertension, however, have a limited capacity to recruit and distend their vasculature and, as a result, may have significant increases in pulmonary artery pressure in response to the increases in blood volume and cardiac output.
Significant upper airway changes also occur in pregnant women including substantial mucosal edema due to an increase in serum estrogen levels as well as capillary engorgement from increased circulating blood volume.7 In the nasal passages, these changes can predispose to epistaxis, while in the oropharyngeal and laryngeal region these changes can increase airflow resistance and predispose to significant difficulties with airway visualization during intubation.
Lower esophageal sphincter function is impaired in pregnant women due to both the effect of increased serum progesterone levels as well as upward displacement of the stomach by the gravid uterus.2,3 As a result, pregnant women are at a greater risk for aspiration compared to non-pregnant women regardless of when they last ate. Risk may be further increased by administration of opiates or other medications that delay gastric emptying.
Transaminase levels are generally unchanged in pregnancy while alkaline phosphatase levels are typically elevated. The latter change is usually not reflective of biliary tract pathology, however, and instead occurs as a result of increased placental production.3,4
Hematologic System and Oxygen Delivery
Red blood cell mass increases during pregnancy by 15%-30%, depending on whether the woman uses iron supplements, but because plasma volume expands to an even greater extent, hemoglobin concentration and hematocrit fall.2 Plasma volume expansion carries the benefit of decreased blood viscosity and improved placental perfusion as well as added protection against blood loss during labor and delivery, but the "physiologic anemia of pregnancy" does decrease arterial oxygen content. Oxygen delivery to the placenta and other organ systems is maintained, however, due to the increase in maternal cardiac output and uterine blood flow described above.
Important changes also occur in the systemic coagulation system. Resistance to activated protein C increases in the latter half of pregnancy while protein S levels decrease. Levels of fibrinogen are increased as are the levels of most clotting factors involved in the clotting cascade.4 These changes induce a hypercoagulable state in pregnant women that, while perhaps protective against excessive bleeding during labor and delivery, likely increases the risk of venous thromboembolism.
As noted above, cardiac output increases significantly over the course of pregnancy. This leads, in turn, to a marked increase in renal blood flow (peaking at 60%-80% above baseline in the second trimester) and an increase in glomerular filtration (50% above pre-pregnancy values by week 16).2 Given these changes, the normal serum creatinine level in a pregnant woman should be lower than that seen in non-pregnant women of similar age and muscle mass. As with "normal" blood pressure observations noted above, seemingly "normal" creatinine levels may actually signify impaired renal function.
A second important change in the renal system involves dilation of the renal pelvis and ureters stemming from both hormonal and mechanical factors.2 As a result of these changes, pregnant women are at increased risk of urinary tract infections including pyelonephritis.
In caring for the pregnant patient it is vital to remember that the fetus is also at stake and recognition of key aspects of fetal and placental physiology can have a big effect on interpretation of maternal data and management decisions. As noted above, 10% (or roughly 500 mL/min) of the cardiac output is delivered to the pregnant uterus near term. Any decrease in cardiac output will cause a decrease in uterine blood flow because the already dilated uterine arterial bed cannot dilate further in response to this insult.2 Hypotension, endogenous or exogenous catecholamines, and maternal alkalosis can also impair uterine blood flow by causing uterine artery vasoconstriction.2,6 Maternal alkalosis further impairs oxygen delivery to the fetus by causing a leftward shift in the hemoglobin-oxygen dissociation curve that limits oxygen off-loading in the placenta.
Oxygen delivered to the placental membrane is passed to the fetus through a countercurrent exchange mechanism. Fetal blood leaves the placenta via the umbilical vein with a PO2 of about 35 mm Hg, then mixes with deoxygenated blood from the fetal inferior vena cava to yield a PO2 of only about 25 mm Hg in the fetal systemic circulation.2
Despite this fantastically low PO2, fetal oxygen content and oxygen delivery are well maintained due to a high fetal cardiac output and hemoglobin concentration, as well as the markedly increased oxygen affinity of fetal hemoglobin. These factors combine to allow the fetus to tolerate significant (perhaps up to 50%) declines in both uterine blood flow and fetal oxygen content before suffering adverse effects.2 It is important to remember, however, that because the fetus is operating on the steep portion of its hemoglobin-oxygen dissociation curve, changes in maternal oxygen tensions that yield even small changes in fetal oxygen tensions can have a large impact on fetal oxygen saturation and tissue oxygen delivery.
In this review, I have considered the basic physiologic changes that occur across multiple organ systems in pregnant women. Awareness of these expected changes, which are summarized in Table 3, and the ability to distinguish normal findings from abnormal findings are critical in the management of these patients. With this knowledge in mind, I will address the main forms of critical illness in pregnant women in a future issue of Critical Care Alert.
Table 3. Summary of changes in major organ systems during pregnancy.