Preeclampsia is defined by the maternal manifestations of hypertension and proteinuria occurring in the second half of pregnancy. The presentation and diagnostic features of preeclampsia are reviewed in Tables 78.2 and 78.3 (12–17). Although hypertension above 140/90 mmHg and proteinuria over 300 mg/24 hr are required for the diagnosis of preeclampsia, some cases may present initially without these features, or may present—as in the case of postpartum eclampsia—after some of these features have already resolved.
Preeclampsia is defined to be severe by the presence of one or more of the following (1):
- Hypertension: systolic above 160 mmHg or diastolic above 110 mmHg on two occasions at least 4 hours apart while the patient is on bed rest
- Thrombocytopenia (platelet count <100,000 cells/µL)
- Impaired liver function (elevated blood levels of liver transaminases to twice the normal concentration)
- Severe persistent right upper quadrant or epigastric pain unresponsive to medication and not accounted for by alternative diagnoses
- New development of renal insufficiency (elevated serum creatinine >1.1 mg/dL, or doubling of serum creatinine in the absence of other renal disease)
- Pulmonary edema
- New-onset cerebral or visual disturbances
Eclampsia results when seizures occur that are not related to other underlying disorders. These features describe a group of patients with an increased risk of fetal and maternal morbidity for whom delivery should be strongly considered. Preeclamptic patients who lack any of the features of severe preeclampsia may have to be observed without moving toward delivery if the fetus is significantly premature and the mother remains under close observation; however, such patients are rarely seen in intensive care settings.
|TABLE 78.2 Clinical Features of Preeclampsia|
Life-threatening maternal complications of preeclampsia such as severe hypertension, seizure, cerebral hemorrhage, pulmonary edema, disseminated intravascular coagulation (DIC), acute renal failure (ARF), and hepatic failure and/or rupture, occur in a minority of cases of preeclampsia. However, these conditions are most likely to require intensive care and are therefore reviewed here in more detail.
|TABLE 78.3 Laboratory Features of Preeclampsia|
A single blood pressure threshold that would absolutely necessitate treatment in the setting of preeclampsia is not established. Expert opinion favors urgent treatment of blood pressures greater than 180 mmHg (systolic) and 110 mmHg (diastolic) and, in the setting of obvious hypertensive end-organ damage (retinal hemorrhage, papilledema, pulmonary edema, severe headache, or renal failure), the blood pressure should be kept under 160/100 mmHg; beyond this consensus, opinions vary considerably (18,19).
Although no evidence suggests that treating blood pressures between 160/100 and 180/110 mmHg in the setting of preeclampsia improves maternal or fetal outcomes, many experts believe that the risks for seizure, placental abruption, stroke, and cerebral hemorrhage are decreased by bringing blood pressures down into the normal or mildly hypertensive range (20). Because preeclampsia is felt to be a dynamic vasospastic disorder with associated target-organ ischemia, some experts suggest letting blood pressures run in a moderately severe range to avoid worsening ischemia in areas of regional vasospasm. In the absence of direct evidence of end–target-organ damage from severe hypertension, it is our practice to treat all blood pressures over 160/105 mmHg. However, although we treat these blood pressures urgently, we are careful to avoid any severe, sudden decreases in maternal blood pressure that may adversely affect uteroplacental and cerebral perfusion.
If urgent blood pressure reduction is required, intravenous labetalol or intravenous hydralazine can be used. Increasing evidence indicates that labetalol may be the better choice of the two; it is our preferred agent, although both agents are still acceptable (20). Hydralazine has been associated with an increased risk of an emergency cesarean in women who receive it while still pregnant and with lower Apgar scores in the infants of mothers who have been given this agent prior to delivery. Short-acting oral nifedipine is also used at some centers as an alternative to labetalol or hydralazine for the acute treatment of severe hypertension. Although its use in medical patients is now discouraged, its use for control of blood pressure in young pregnant or postpartum women without coronary artery disease remains an acceptable practice. Previous concerns about a drug interaction between magnesium and calcium channel blockers appear to be ill-founded (21). Diuretics should not be used in this setting unless pulmonary edema is present because, despite the edema that is so common in preeclamptic patients, most hemodynamic studies of preeclamptic women suggest that they are actually intravascularly volume depleted.
Once the patient has delivered, any antihypertensive agent can be used for blood pressure control. At that point, nitroprusside and nitroglycerin are excellent choices because of their very short half-lives.
Seizures are the most well-known severe manifestation of preeclampsia. The risk of an eclamptic seizure in a patient with untreated preeclampsia is estimated to be about 1 in 200. Because of early identification of preeclampsia and the widespread use of magnesium prophylaxis, the incidence of eclampsia in the United States ranges from 1 in 1,000 to 1 in 20,000 deliveries; when it does occur, eclampsia is associated with a maternal mortality rate of 5% and a perinatal mortality rate between 13% and 30%.
Eclamptic seizures are typically of the grand mal variety, with clonic–tonic muscular activity followed by a postictal period. However, focal, jacksonian-type and absence seizures have been described. Most eclamptic seizures occur in the setting of established preeclampsia with hypertension and proteinuria. Classically, they are preceded by evidence of neuromuscular irritability such as tremulousness, agitation, nausea, vomiting, and/or clonus. However, some patients will present with seizure as their first manifestation of preeclampsia, usually occurring in the absence of hypertension or proteinuria.
The onset of eclamptic convulsions can be antepartum (38% to 53%), intrapartum (18% to 36%), or postpartum (11% to 44%). Postpartum eclamptic seizures generally occur in the first 48 hours after delivery, but it is not unusual to see them occur anytime in the first week after delivery; eclamptic seizures have been reported as late as 23 days postpartum.
The underlying pathophysiology of the eclamptic seizure is unclear. They cannot be attributed simply to severe hypertension, because eclampsia can be seen in patients with only mild elevations in blood pressure. Electroencephalograms may show epileptiform abnormalities, but usually show only a nonspecific diffuse slowing that may persist for weeks after delivery. Computed tomography (CT) and magnetic resonance imaging (MRI) of the eclamptic patient can be normal, or may show findings ranging from diffuse edema to focal areas of hemorrhage or infarction. Symmetrical white matter edema in the posterior cerebral hemispheres, particularly the parieto-occipital regions is characteristic for reversible posterior leukoencephalopathy syndrome (RPLS). Some suggest that RPLS could be considered an indicator of eclampsia, even when the other features of eclampsia (proteinuria, hypertension) are not present. MRI is more sensitive in detecting abnormalities in eclamptic patients, but both CT and MRI of the brain can be normal, particularly if done in the first 24 hours after the seizure. When radiologic changes are present, some—but not all—of these changes usually resolve with time (22).
Management of Eclamptic Seizures
Even when delivery is impending, a preeclamptic woman should still receive an anticonvulsant to prevent eclamptic seizures; magnesium sulfate is the medication of choice for this purpose (23). It halves the risk of eclampsia in patients with preeclampsia and lowers the risk of recurrent seizures and maternal death in women with eclampsia. It is superior to phenytoin and benzodiazepines in preventing further seizures. Magnesium is typically given as an intravenous bolus of 4 to 6 g, followed by a continuous intravenous infusion of 1 to 4 g/hr. Either monitoring plasma concentrations (which should run between 4 and 7 mmol/L), or observing the patient closely for symptoms and signs of toxicity (hypotension, hypotonia, muscular weakness, and respiratory depression) are reasonable options. Carefully monitoring for toxicity is important, particularly in patients with worsening renal function. Severe respiratory depression in a patient on magnesium should be treated with intravenous calcium. The only role of magnesium in preeclampsia is that of an anticonvulsant. Despite the possibility of a transient decrease in blood pressure with its initial administration, magnesium has no significant sustained effect on blood pressure. Its mechanism of action remains unclear, but it does not seem to have any intrinsic anticonvulsant effect, and may actually prevent seizures through its action as a cerebral vasodilator.
If the woman does have an acute eclamptic seizure, intravenous benzodiazepine is indicated to acutely stop the seizure, and magnesium should then be initiated if this has not already occurred. If an eclamptic convulsion occurs while a patient is receiving magnesium, most clinicians will add phenytoin to the regimen. Continued seizures should warrant the involvement of neurology and consideration of the use of other antiepileptic drugs. Anticonvulsant therapy can generally be stopped once postpartum diuresis has begun and the manifestations of preeclampsia have started to improve.
Neuroimaging with CT or MRI is recommended for most patients with eclamptic seizures to rule out an intracerebral hemorrhage. The timing of these neuroimaging tests should be determined by the level of clinical suspicion for this diagnosis, and should not substantially delay delivery.
Cerebrovascular accidents are three to seven times more common in pregnancy. Preeclampsia accounts for over a third of the strokes that do occur during pregnancy, and at least half of the deaths from preeclampsia in the developed world are due to stroke. Most of the strokes in patients with preeclampsia will be related to intracerebral hemorrhage, but can also occur due to vasospastic ischemia (24). Preeclampsia-related stroke is often, but not always, associated with severe hypertension and/or eclamptic convulsions. Sudden onset or worsening of a headache, a change in mental status, or any focal neurologic complaint occurring in the context of preeclampsia should lead to consideration of this diagnosis and urgent neuroimaging.
Pulmonary edema occurs in about 3% of cases of preeclampsia, and can cause significant maternal morbidity (25–27). It occurs as a result of the interplay of preeclampsia-related pulmonary endothelial damage and the low plasma oncotic pressure seen in all pregnancies; excessive intravenous fluid is also, typically, a contributing factor. It is often seen in the postpartum period after a patient has received a substantial amount of intravenous fluid in labor (or with cesarean delivery) and when mobilization of fluid from the involuting uterus begins. Pulmonary edema in this setting is often amenable to gentle diuresis but may be severe enough to warrant mechanical ventilation.
Echocardiographic studies demonstrate that transient systolic or diastolic ventricular dysfunction is present in up to one-third of preeclampsia cases associated with pulmonary edema. This preeclampsia-related myocardial dysfunction is believed to be a manifestation of vasospastic coronary ischemia, and usually resolves rapidly with resolution of the preeclampsia. We consider this to be a distinct entity from peripartum cardiomyopathy (PPCM) and do not believe there is a substantial recurrence risk of cardiac disease for these patients in a subsequent pregnancy.
Prevention and Treatment of Pulmonary Edema
It is important to avoid excessive fluid administration to patients with preeclampsia because of their propensity for pulmonary edema. Ideally, one individual should be designated to approve and monitor all fluid administration in these patients. Regular auscultation of the lungs and use of transcutaneous pulse oximetry in patients with severe preeclampsia will help identify cases of pulmonary edema as they evolve. This careful observation should be continued in the postpartum period because pulmonary edema often occurs as late as 2 to 3 days after delivery. Acute treatment of pulmonary edema should involve supplemental oxygen, low-dose furosemide, and, if needed, morphine (27,28). Blood pressure control may help treat pulmonary edema by decreasing afterload. An echocardiogram should be obtained to look for an underlying cardiac contribution. Intubation and mechanical ventilation may become necessary if the above measures do not improve the patient’s oxygenation.
Disseminated Intravascular Coagulation
Disseminated intravascular coagulation (DIC) can occur as a late and severe complication of preeclampsia or eclampsia (29). Because most patients with preeclampsia-related DIC have low platelet counts or elevated transaminase levels, DIC screening in the absence of these abnormalities is generally not necessary (30). However, a DIC screen should be ordered in all preeclamptic patients with rising liver enzymes, dropping platelet counts, and/or any abnormal bleeding. This is particularly important if there is a possibility of an operative delivery.
Acute Renal Failure
Preeclampsia is often associated with a mild degree of renal impairment manifesting as a slightly elevated creatinine or a decreased urine output. This is due to a combination of intravascular volume depletion, renovascular vasospasm, and a preeclampsia-related glomerular lesion known as glomerular endotheliosis. This mild renal impairment usually resolves rapidly after delivery.
Acute renal failure in preeclampsia is not common. If it does occur, acute tubular necrosis (ATN) and partial or total cortical necrosis are the most likely underlying lesions, and are thought to be caused by preeclampsia-related, vasospasm-induced renal ischemia. A history of transient hypotension is also typically present in these cases. The differential diagnosis includes ATN from sepsis or hemorrhage, or renal failure from causes unassociated with pregnancy such as hemolytic uremic syndrome, medication effects, or acute glomerulonephritis.
Most renal failure in the setting of preeclampsia is rapidly reversible, but if significant hypotension has occurred (as may happen with placental abruption or DIC-related hemorrhage), ATN or renal cortical necrosis may result and necessitate dialysis. In persons with sustained oliguria in the setting of preeclampsia, fluid challenges should be given cautiously because of the risk of pulmonary edema. Poor outcomes in preeclampsia are far more commonly related to pulmonary edema than they are to decreased urine output. Diuretics to improve urine output should be avoided in the absence of pulmonary edema because of the intravascular volume depletion present in most patients with preeclampsia.
If the patient is unresponsive to small fluid boluses, the use of central venous pressure (CVP) monitoring may be a helpful, if not completely reliable, guide. The role of the pulmonary artery catheter in this context is unproven, and should only be used by nurses and physicians who are trained and experienced in its use. Increasing data from randomized control trials have shown that pulmonary artery catheters are of less benefit than previously believed in nonpregnant patients, and there is little reason to believe this tool has a uniquely beneficial role in the pregnant population.
Sustained oliguria in preeclampsia is unusual, and therefore significant and rapid peripartum renal deterioration should also lead to consideration of differential diagnoses that include the hemolytic uremic syndrome (HUS), thrombotic thrombocytopenic purpura (TTP), and renal cortical necrosis. It is therefore advisable to perform careful microscopic examination of urinary sediment and a peripheral smear in all pregnant or postpartum patients with oliguria (31).
A distinct clustering of the manifestations of preeclampsia is the HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet counts). This constellation of findings represents a particularly severe form of preeclampsia with significant risk for maternal illness and fetal injury or death (32,33). HELLP occurs in up to 20% of cases of severe preeclampsia. The hemolysis is microangiopathic, and therefore schistocytes (fragmented erythrocytes) are seen on peripheral smears of the blood. Lactate dehydrogenase levels are usually increased and liver enzyme elevation may be two- to threefold. The thrombocytopenia can be precipitous and severe. High-dose dexamethasone is often given to treat patients with HELLP, but it is not clear that this intervention has clinically significant effects on outcomes, and the treatment remains supportive care coupled with delivery (34,35).
Hepatic Rupture, Infarction, or Hemorrhage
Epigastric or right upper quadrant pain and elevation of hepatic enzymes due to preeclampsia are common. When these factors are present, it suggests severe disease and preeclampsia-related hepatic edema and ischemia. It generally is associated with no more than a two- to fourfold increase in aspartate aminotransferase (AST) or alanine aminotransferase (ALT). When pain is severe and/or hepatic enzymes rise above this level, preeclampsia-related hepatic infarction, hemorrhage, and rupture should be considered and investigated with a hepatic ultrasound or CT (36). Acute fatty liver of pregnancy (AFLP) is also part of the differential diagnoses in these cases.
Diabetes insipidus is a rare complication of preeclampsia with significant hepatic involvement. It can also be seen with AFLP. It has been hypothesized that the acute liver dysfunction in these patients reduces the degradation of vasopressinase (an enzyme which itself degrades vasopressin), and results in a state of relative vasopressin deficiency (37). The course of the condition follows that of the underlying disorder and can be treated with additional vasopressin until it resolves.
The Role of Arterial Lines, Central Venous Pressure Monitors, and Pulmonary Artery Catheters in Preeclamptic Patients
Most severe preeclamptic patients have normal or hyperdynamic left ventricular function with normal pulmonary artery pressure. Thus, a CVP monitor usually is adequate to assess volume status and left ventricular function. However, severely preeclamptic patients may develop cardiac failure, progressive and marked oliguria, or pulmonary edema. In such cases, some authors suggest that a pulmonary artery (PA) catheter may be helpful for proper diagnosis and treatment, because right and left ventricular pressures may not correlate (38,39). Given that evidence has evolved that the routine use of pulmonary artery catheters may not be as beneficial in the care of nonobstetric patients as once believed, the rather limited literature about their use in obstetric populations cannot help but be questioned (40–42). No clear consensus exists as to their role in the management of preeclampsia (43). We rarely employ them in any obstetric patients, as the risks—especially on labor and delivery units where the personnel have less experience in their placement and interpretation—seem to outweigh the evidence justifying their use. When questions arise as to whether cardiac dysfunction is contributing to a preeclamptic patient’s pulmonary edema and/or renal failure, we obtain an urgent bedside echocardiogram to guide our care and, in the absence of a significant cardiac cause, manage these patients clinically.
An intra-arterial catheter monitor may be indicated for protracted severe hypertension during therapy with potent antihypertensive agents or when there is a significant disparity between automated and manual cuff measurements of blood pressure.
Cardiac disease during pregnancy has an incidence rate of 0.4% to 4%, and is associated with a maternal mortality of 0.4% to 6%, depending on the cardiac lesion being discussed (44). Indeed, it is now the leading cause of maternal mortality in North America (45). Although rheumatic heart disease is far less of a concern in the West than it was several decades ago, it remains a problem, along with peripartum cardiomyopathy, pulmonary hypertension, adult congenital heart disease, and myocardial ischemia. These conditions will be the focus of this section. Although many of the patients with cardiac disease who end up under the care of a critical care physician will have cardiac disease that was identified prior to pregnancy, a significant portion of patients will also have their cardiac disease present for the first time during pregnancy. The physiologic changes of pregnancy may exacerbate, and thereby unmask, previously undiagnosed cardiac disease, and pregnancy can predispose patients to the onset of certain cardiac diseases such as PPCM or ischemic heart disease. Some of the physiologic changes associated with pregnancy are reviewed below and are summarized in Table 78.4.
Maternal blood volume gradually increases during pregnancy to 150% of nonpregnant levels (46). The increase in plasma volume (45% to 55%) is greater than the increase in red blood cell volume (20% to 30%), resulting in a relative anemia of pregnancy. This increase in blood volume is associated with an increase in cardiac output (CO), which begins early in gestation and peaks at levels 30% to 40% over nonpregnant values between 20 and 30 weeks (46); the increase then plateaus until term. CO in a twin pregnancy is 15% higher than that of a singleton pregnancy (47).
The increase in CO with gestation is dependent on heart rate and stroke volume. Heart rate gradually increases throughout pregnancy, starting as early as 4 weeks of gestation, with a 10% to 15% increase by term. Stroke volume, in contrast, peaks during the second trimester, with a 20% to 40% increase over the nonpregnant state.
During labor, CO rises another 15% to 45% above prelabor values with an additional increase of 10% to 25% during uterine contractions. The increase in CO in labor during contractions versus that seen between contractions is greater late in the first stage (34%) versus early in the first stage (16%) (48).
Oxygen consumption increases 20% during pregnancy, and may increase as much as 40% to 100% during active labor. In the immediate postpartum period, CO increases 30% to 40% over the labor period or 60% to 80% over the nonpregnant state, with the increased blood volume shifting to the central circulation from the contracted uterus, as well as alleviation of aortocaval compression and a slight decrease in total peripheral resistance.
|TABLE 78.4 Hemodynamic Changes in Pregnancy|
CO and other hemodynamic parameters are thought to return to their baseline prepregnant state by 6 weeks after delivery. However, CO may remain elevated for up to 12 weeks (49).
Systemic arterial pressure decreases by 10 to 15 mmHg over the first two trimesters and then gradually returns to baseline by term. Systemic vascular resistance decreases 10% to 20% during pregnancy. Moreover, systemic vascular resistance may remain decreased for at least 12 weeks postpartum.
Venous pressure in the lower extremities increases and peaks near term as the gravid uterus compresses the inferior vena cava—especially when the patient is supine—while CVP remains unchanged. Total-body water increases by about 2 kg throughout pregnancy.
Invasive PA catheterization in low-risk, near-term pregnant patients (36 to 38 weeks) reveals a significant decrease in pulmonary vascular resistance, colloid oncotic pressure (COP), and COP–pulmonary artery occlusion pressure (PAOP) gradient, with no change in PAOP or left ventricular stroke work index (50).
With a significant increase in oxygen consumption, especially during labor, along with a decrease in functional residual capacity, the importance of adequate preoxygenation (denitrogenation) before rapid sequence induction of anesthesia cannot be overemphasized. Morbidity and mortality statistics from England and Wales reveal that anesthetic-related maternal mortality is predominantly caused by the inability to intubate the trachea or by pulmonary aspiration during general anesthesia (51). Thus, an awake orotracheal intubation should be considered when airway patency is suspect. The most experienced person available should typically be the individual who intubates pregnant women on a regular basis.
Despite an average 200- to 500-mL blood loss for routine, uncomplicated vaginal deliveries and an 800- to 1,000-mL blood loss for cesarean section deliveries, blood transfusions are seldom necessary because of the increased blood volume and the autotransfusion of approximately 500 mL of blood from the contracted uterus in the postpartum period. Although this increase in blood volume protects against blood loss at delivery, pulmonary congestion and cardiac failure can result in patients with underlying cardiac dysfunction.
Pregnant women have a predisposition to pulmonary edema. Physiologic changes in pregnancy that favor the development of pulmonary edema include an increase in intravascular volume, decreased blood viscosity (“physiologic anemia of pregnancy”), decreased COP, and fluid shifts, especially in the immediate postpartum period.
Patients with minimal cardiac reserve may tolerate early pregnancy, and subsequently decompensate from increasing blood volume and the need for an increased CO in the late second trimester and early third trimester. Patients with moderate cardiac reserve may tolerate pregnancy well until labor and delivery or the puerperium. Thus, cardiac patients should continue to be closely monitored in the postpartum period because cardiac decompensation most frequently occurs during this time; the prepregnant baseline state may not be reached for as long as 12 weeks after delivery.
The enlarging uterus in the third trimester predisposes to aortocaval compression and decreased CO in supine patients. Inferior vena cava compression occurs in up to 90% of near-term parturients in the supine position. However, only about 10% to 15% of patients manifest the supine hypotensive syndrome because of shunting of venous blood away from the caval system to the azygos system by the intervertebral plexus of veins. Patients most susceptible to supine hypotension are those with polyhydramnios and multiple gestation. However, in most patients in the lateral position, CO is maintained. Turning from the supine to the lateral decubitus position increases CO from 8% at 20 to 24 weeks to as much as 30% near term (52). Therefore, to avoid aortocaval compression, measures such as uterine displacement by maternal position (lateral decubitus), bed position (left lateral tilt), or uterine displacement devices are imperative, especially in the last trimester. Moreover, maternal hypotension and placental hypoperfusion from aortocaval compression can be compounded by regional anesthesia that interferes with compensatory sympathetic nervous system mechanisms (53).
As a consequence of these cardiovascular changes, normal symptoms of pregnancy can include fatigue, dyspnea, decreased exercise capacity, and lightheadedness. Cardiac signs that may be seen in normal pregnancies include distended neck veins, peripheral edema, loud first heart sound, loud third heart sound, systolic ejection murmurs, and continuous murmurs (cervical venous hums and mammary souffle). Fourth heart sounds and diastolic murmurs occur rarely in normal pregnancy and should be considered pathologic unless proven otherwise. These changes are reviewed in Table 78.5. Therefore, the normal signs and symptoms of pregnancy may simulate pathologic disease states, thereby rendering the diagnosis of heart disease difficult.
|TABLE 78.5 Normal Cardiac Symptoms and Signs in Pregnancy|
Normal chest radiographic findings demonstrate increased lung markings (prominent pulmonary vasculature partly due to both increased blood volume and increased breast shadow). Electrocardiographic (ECG) changes may include a left QRS axis deviation and nonspecific ST-segment and T-wave changes.
Who Is Most at Risk and When Is That Risk Greatest?
Table 78.6 classifies the risk of various cardiac lesions in pregnancy. When we speak about “risk” for these patients, we refer to congestive heart failure, arrhythmias, stroke, and death. Overall, about 13% of cardiac patients will suffer one of these outcomes in pregnancy. The presence of pulmonary hypertension is always associated with an increased risk, and this risk is commensurate to its degree of severity. Other factors associated with an increased risk of cardiac complications in pregnancy include the following (54):
|TABLE 78.6 Peripartum Risk of Various Cardiac Lesions|
- New York Heart Association (NYHA) functional class. This is perhaps the most important predictor of pregnancy outcome. Patients with NYHA class I and II cardiac disease generally have a good prognosis during pregnancy. Patients with NYHA class III and IV are more likely to experience complications and may require special management around the time of delivery.
- Left-sided obstructive cardiac lesions. Patients with lesions such as aortic stenosis may have difficulty accommodating the increased blood volume and CO seen in pregnancy, and become increasingly symptomatic. Interestingly, patients with regurgitant valvular lesions may have less difficulty in pregnancy, as CO in these cases may benefit from the decrease in systemic vascular resistance seen in pregnancy.
- Left ventricular systolic dysfunction
- Prior cardiac events or previous dysrhythmia
Although pregnant women with cardiac disease may experience complications at any point during pregnancy, there are three periods of particular risk:
- At the end of the second trimester, when CO has increased to its peak
- At the time of labor and delivery, when cardiac work may be increased dramatically by both pain and the autotransfusion of blood from the placenta and uterus with each contraction
- In the first 72 hours following delivery, when the uterine involution and resolution of pregnancy-related edema leads to mobilization of large amounts of fluid
General Management of Cardiac Patients During Pregnancy
Management of patients with cardiac disease in pregnancy should, in general, include good preconception counseling to assess and inform the patient of the risks associated with a pregnancy. Although no woman should be told that she “should never get pregnant,” a clear discussion of the risk is essential. With cases such as severe pulmonary hypertension or Eisenmenger syndrome, the patient should be strongly cautioned against pursuing a pregnancy. Women with congenital heart disease need also be informed that they are at increased risk of giving birth to a child with congenital heart disease. If a woman with cardiac disease decides to pursue a pregnancy after a clear discussion of risk, the cardiologist should ensure that her cardiac status is clearly delineated and optimized. Ideally, any necessary investigations or interventions should be carried out prior to conception. Once a woman is pregnant, regular visits with a medical specialist and an obstetrician trained in the care of high-risk pregnancies to watch for evidence of heart failure and arrhythmias are essential. Consultation with an obstetric anesthesiologist prior to delivery is also prudent.
As stated earlier, most cardiac medications can be used in pregnancy when indicated. Table 78.7 lists many common cardiac medications, and classifies them as to which drugs we know the most about regarding their safe use during pregnancy and which drugs we know the least. However, it should be emphasized that among the more commonly used cardiac medications, only angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and warfarin are known or strongly suspected to be human teratogens. Amiodarone has had mixed data with respect to its safety in pregnancy, with some reports of congenital hypothyroidism, goiter, prematurity, hypotonia, and bradycardia (55,56). Although use in an acute setting is appropriate, it is not a first-line agent for maintenance therapy in pregnancy. Angiotensin-converting enzymes and angiotensin receptor blockers both have been associated with fetal anomalies, fetal loss, oligohydramnios, cranial ossification abnormalities, and neonatal renal failure. Although their use in the first trimester was once supported, recent evidence suggests they should not be used at any time in gestation (57). Warfarin is associated with a high risk of miscarriage and anomalies of the eyes, hands, neck, and central nervous system (58). Again, the guiding principle of managing critical illness in pregnancy should be that, because fetal well-being depends on maternal well-being, medications that are of benefit to maternal health should also be considered to be in the fetus’ best interest. Useful sources for reviewing the available safety data for medications during pregnancy and with breastfeeding are found in references (59–65).
|TABLE 78.7 Commonly Used Cardiac Medications and Their Safety in Pregnancy|