Page 1786 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 127: Critical Illness in Pregnancy 1255

increase another 10% to 15% due to increased blood return from uter- somewhat decreased in normal pregnancy, the drop in bicarbonate is
ine contractions, and to pain-mediated sympathetic stimulation. This not associated with a substantial change in the anion gap.
effect on cardiac output may be tempered by blood loss during delivery. Due to augmented minute ventilation, the maternal arterial partial
In healthy women, there is no substantial change in the properties of pressure of oxygen (Pa O 2 ) is increased throughout pregnancy to greater
ventricular contractility over the course of pregnancy. 4-6,8 Cardiac output than 100 mm Hg. As it does not alter the degree of hemoglobin satura-
in pregnancy can be highly dependent on body position; vena caval and tion, this increase in Pa O 2 does not significantly increase oxygen delivery.
aortic obstruction by the gravid uterus is maximal in the supine posi- An increased alveolar-to-arterial oxygen gradient [(A − a) O 2 ] with mild
tion but is much less pronounced in the left lateral decubitus position. hypoxemia may occur in the supine position. Whenever possible, arte-
2
16
Obstruction of the inferior vena cava results in reduced venous return, rial blood gas samples should be obtained in the seated position to avoid
and obstruction of the abdominal aorta results in increased afterload. the confounding effect of positional hypoxemia.
These effects on cardiac output are most notable in the third trimester. Lung compliance is unchanged in pregnancy. However, elevation of
Blood pressure decreases early in pregnancy, reaching a nadir the diaphragm from the enlarging uterus leads to decreased chest wall
between 16 and 28 weeks, and then gradually increases. Blood pres- compliance. This results in a progressive decline in the functional resid-
9
sure returns to prepregnancy levels shortly after delivery. Hypertension ual capacity (FRC), which reaches a 10% to 25% reduction by term.
3,15
in pregnancy is defined by systolic pressures >140 mm Hg or diastolic Expiratory reserve volume and residual volume are de
https://kat.cr/user/tahir99/creased during
pressures >90 mm Hg. Systolic pressures ≥160 mm Hg or diastolic pres- the second half of pregnancy. Total lung capacity, however, decreases
15
sures ≥110 mm Hg define severe hypertension, and require treatment. 10 minimally as respiratory muscle function is unimpaired, and widening
The normal adaptation of the circulatory system to pregnancy results of the thoracic cage increases inspiratory capacity. 12,15 Vital capacity also
in a physiologic third heart sound in many patients. The chest radio- remains unchanged during pregnancy. Diffusing capacity is unchanged
graph reveals an enlarged cardiac silhouette due to increased circulating or slightly increased early in pregnancy and then decreases to normal
blood volume and cardiac filling. The pulmonary artery and right ven- or slightly below normal after the first trimester. Airway closure may
17
tricular pressures are unchanged, with a hormone-mediated reduction occur near or above FRC in some women late in pregnancy. 17,18 The
in pulmonary vascular resistance compensating for the increased flow decrease in FRC combined with an increase in oxygen consumption
from augmented cardiac output. The pulmonary artery wedge pressure make the pregnant woman and the fetus more vulnerable to hypoxia
(Ppw) also is generally unchanged from prepartum values. 3,11 in the event of hypoventilation or apnea. This is an important consid-
■ ADAPTATION OF THE RESPIRATORY SYSTEM eration during endotracheal intubation. Despite increases in several
hormones known to affect smooth muscle, airway function does not
Oxygen consumption is increased by 20% to 35% in normal pregnancy, appear to be altered in pregnancy. Accordingly, the forced expiratory
and rises even further during labor (Table 127-2). 12,13 Increased oxygen volume in 1 second (FEV ), the ratio of FEV to forced vital capacity,
1
1
consumption is the result of fetal and placental utilization, as well as and the airways resistance are unchanged. The fact that flow-volume
increased maternal requirements from increased cardiac output and loops are also unaffected by pregnancy is further evidence of normal
work of breathing. Increased oxygen consumption is associated with airway function. 19
13
an increase in carbon dioxide production, which reaches 34% to 50%
above baseline by the third trimester. Minute ventilation increases early ■ RENAL AND GASTROINTESTINAL ADAPTATION
in pregnancy and peaks at 20% to 40% above baseline at term. The Renal blood flow increases throughout the first and second trimesters
3,14
increased ventilation is above the level needed to eliminate carbon diox- to reach 60% to 80% above prepregnancy levels. The glomerular filtra-
3
) is reduced
ide, and the arterial partial pressure of carbon dioxide (Pa CO 2 tion rate rises early in pregnancy to 50% above baseline, and remains
to 27 to 34 mm Hg throughout pregnancy. Augmented ventilation is increased throughout pregnancy. Therefore, the usual serum creatinine
20
attributed to respiratory stimulation from progesterone, and results is 0.5 to 0.7 mg/dL, and creatinine levels that would be normal in a non-
from an increase in tidal volume while the respiratory rate is essen- pregnant patient can indicate renal dysfunction in a pregnant patient.
tially unchanged. Renal compensation is associated with a decrease Serum aminotransferases and bilirubin are unchanged in normal
3,15
in serum bicarbonate to 18 to 21 mEq/L, and results in a maternal pH pregnancy. Alkaline phosphatase, produced by the placenta, increases
that is only slightly alkalemic at 7.40 to 7.45. As sodium levels are also throughout pregnancy, peaking at two to four times normal at term. The
concentration of serum albumin is mildly decreased throughout preg-
nancy as a result of hemodilution. Symptomatic gastroesophageal reflux
TABLE 127-2 Respiratory Changes in Pregnancy is common during pregnancy, although basal gastric acid secretion and
21
Parameter Change Time Course pH remain unchanged. The lower esophageal sphincter tone decreases
during the first trimester and remains low until near term, perhaps as a
Oxygen consumption Increases 20%-35% Peak at term result of increased progesterone. The gravid uterus displaces the stom-
Tidal volume Increases 30%-35% Peak at term ach, further reducing the effectiveness of the gastroesophageal sphincter.
Respiratory rate Unchanged In addition to sphincter incompetence, labor and narcotic analgesics
contribute to an increased risk of aspiration from delayed gastric emp-
Minute ventilation Increases 20%-40% Peak at term tying. When being evaluated for intubation, pregnant patients are con-
Total lung capacity Unchanged sidered to have a full stomach, regardless of the timing of the last meal.
Chest wall compliance Decreases ■
Lung compliance Unchanged FETAL OXYGEN DELIVERY
Functional residual capacity Decreases 10%-25% Peak at term Fetal oxygen delivery is determined by uterine artery blood flow, mater-
, and the hemoglobin concentration (Fig. 127-1). Numerous
3
Forced vital capacity Unchanged nal Pa O 2
factors affect uterine artery blood flow. The uterine vasculature is
FEV1 Unchanged maximally dilated under normal conditions and, therefore, is unable to
22
Diffusing capacity Unchanged adapt to stress by increasing flow through local vascular adjustment.
However, fetal oxygen delivery can be decreased by uterine artery
Expiratory reserve volume Decreased 2nd half of pregnancy
vasoconstriction. Exogenous or endogenous sympathetic stimulation,
Residual volume Decreased 2nd half of pregnancy maternal hypotension, and maternal alkalemia elicit uterine artery
FEV1, forced expiratory volume in 1 second. vasoconstriction. 3

section11.indd 1255 1/19/2015 10:52:18 AM