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pregnancy. High-risk patients not taking warfarin should receive For pain relief in labor, epidural analgesia is a good choice for
continuous UFH keeping aPTT levels around two to three times patients with MVP and MR. Avoid epinephrine-containing local
control.21,66 Low-risk women can receive subcutaneous heparin. anesthetics in patients with dysrhythmias.
In the absence of bleeding, heparin or warfarin can be restarted Regional anesthesia for C/S in parturients with MVP has
four to six hours after delivery.21 Some institutions use LMWH been reported.81 Adequate volume loading prior to placement of a
maintaining peak anti-Xa levels between 0.8 to 1.5 and trough regional anesthetic is necessary to avoid LV volume reduction and
levels at least 0.7.77 Anti-Xa levels should be checked twice an increase in MV prolapse. Light GA accompanied by tachycardia



10
Chapter 1


can increase MVP.73 Drugs that cause tachycardia should be mortem studies show enlarged hearts that are soft, flabby, and
avoided. Shivering and peripheral vasoconstriction can increase dilated with variable endocardial thickening or areas of myocar-
LV systolic pressure and increase regurgitant flow. Hence, it is dial necrosis. Endocardial biopsy can be considered in patients
important to maintain normothermia and treat regional anesthe- without improvement after one to two weeks of maximal medical
sia-induced shivering with i.v. meperidine 12.5“25 mg. therapy to help diagnosis and exclude other causes of dilated
cardiomyopathy.84,89 Mortality ranges from 15“50%, with death
resulting from cardiac failure, dysrhythmia, or thromboembo-
Cardiomyopathy in pregnancy
lism.87,91 Peripartum cardiomyopathy can be associated with
pulmonary hypertension and may result in multiorgan failure.92
Currently, nearly 8% of pregnancy-related deaths are caused by
cardiomyopathy,82,83 and this number appears to be increasing. The prognosis is worse if the cardiac size has not returned to
Cardiomyopathy in pregnancy can be divided into peripartum normal within six months of delivery.
cardiomyopathy and other cardiomyopathy (dilated, hyper-
trophic obstructive, or restrictive).82
Management principles
Initial treatment is similar to the management of any form of
Peripartum cardiomyopathy
heart failure.87,93
 Reduce and optimize preload with sodium and fluid-intake
Peripartum cardiomyopathy (PPCM) is defined by the National
Institutes of Health and is based on four criteria:13,84,85,86 restriction and diuretics. Loop diuretics appear safe during
pregnancy, but spironolactone should be avoided.93
 development of cardiac failure in a six-month period (last
 Afterload reduction is the mainstay of medical management.
month of pregnancy to within five months after delivery)
 no identifiable cause Nifedipine, amlodipine, nitroglycerin, and hydralazine have
 new diagnosis with no prior heart disease before the last month all been used. Although ACE inhibitors are contraindicated in
of pregnancy pregnancy due to fetal renal teratogenicity, they may be con-
sidered postpartum and appear safe during breast-feeding.93,94
 echocardiographic findings of LV dysfunction similar to dilated
 Any vasodilator may compromise utero-placental blood flow
cardiomyopathy: ejection fraction <45% and a LV end diastolic
dimension >2.7 cm/m2. and i.v. vasoactive medication administration requires invasive
Peripartum cardiomyopathy accounts for 70% of the pregnancy- monitoring.
 Consider inotropic support. Digoxin and, if necessary, dopa-
related deaths from cardiomyopathy and is one of the leading
causes of maternal death.82,87 The condition is fatal in 15“50% of mine, dobutamine, and milrinone can be considered.95,96 Beta-
cases and the risk of death is higher in black women (six times), blockers have been shown to improve outcome in dilated
women >35 years of age, and in multiple gestation.82 Fortunately, cardiomyopathy.
 Aggressive use of implantable defibrillators has reduced the
mortality rates from PPCM appear to have decreased in the past
risk of sudden death in these patients.88
decade, most likely related to advances in medical therapy for
heart failure.88  Anticoagulation: PPCM has a high rate of thromboembolism
In addition to PPCM, there are a number of causes of dilated due to bed rest, hemoconcentration from diuresis, and subop-
timal CO.93 Anticoagulation is important, especially if LVEF is
cardiomyopathy. Possible etiologies include ischemia, alcohol-
<20%.87 Echocardiographic evidence of intraventricular
ism, toxins, thiamine deficiency, connective tissue diseases,
thrombi should prompt anticoagulation therapy.97
metabolic disorders, neuromuscular dystrophies, and viral or
 Immunosuppressive therapy in PPCM is not yet fully under-
other infections. When no identifiable cause is found, PPCM or
stood,98 but should be considered in patients not responding
idiopathic dilated cardiomyopathy should be considered.
Idiopathic dilated cardiomyopathy appears to be a separate syn- to conventional medical therapy with myocarditis proven on
drome from PPCM.89,90 cardiac biopsy.84 In one series, 78% of women with PPCM had
evidence of myocarditis.99 Immunosuppressive therapy with
Symptoms and signs of heart failure often develop insidiously
and must be distinguished from the normal physiologic changes oral prednisone and azathioprine for six to eight weeks, led to a
resolution of the myocarditis and improved LV function.99
of pregnancy. Women present with fatigue, dyspnea, orthopnea,
palpitations, and hemoptysis. Patients with PPCM often have a Recently, i.v. immunoglubulin therapy has been used success-
fully in PPCM.100
raised jugular venous pressure and new regurgitant murmurs
 Pentoxyfylline therapy (TNF-alpha production inhibitor) has
with a third heart sound or gallop rhythm. A chest radiograph
reveals cardiomegaly and signs of heart failure, while the electro- also been used for PPCM with improvement in the 30 patients
treated.101 Continuous veno-venous hemofiltration has been
cardiogram (ECG) may show dysrhythmias with nonspecific
ST- and T-wave changes. Echocardiography confirms dilated used successfully to treat severe cardiomyopathy after failure
of conventional therapy.96 There is also an isolated report
hypokinetic ventricles. Serial echocardiographic studies during
pregnancy and the postpartum period to monitor LV function are of a successful treatment of PPCM with daily exchange
recommended.91 transfusions.102
 Heart transplantation is reserved for severe cases unresponsive
The cause of PPCM is unknown. Hypotheses include myo-
carditis secondary to a viral or autoimmune response.84 Post- to all medical therapy103 and has been performed successfully



11
1 Cardiovascular and respiratory disorders


in patients with PPCM.104,105,106 Intraaortic balloon pump or on exertion, angina, and syncope). Some patients with HOCM
ventricular assist devices have been used as a bridge to cardiac may deteriorate and progress to congestive heart failure.
transplant.95,104,105,106 Clinically, patients have signs of LV hypertrophy with a late sys-
tolic murmur at the apex.
Hypertrophic obstructive cardiomyopathy is a disease trans-
Anesthetic options
mitted by autosomal dominant inheritance with variable pene-
If patients can be stabilized on medical therapy, induction of tration. Asymmetrical septal and LV hypertrophy are hallmarks of
labor is recommended. However, if the woman™s condition wor- this disease, causing a dynamic outflow tract obstruction during
sens, C/S should be considered since she may not tolerate a systole. Obstruction to LV outflow is caused by a hypertrophic
prolonged stressful labor. Consider invasive monitoring appro- muscle mass at the base of the interventricular septum. There is
priate for the patient™s condition.107 Early administration of a an apical obliterative variety, which does not have a subaortic
labor epidural is important to minimize the stress of labor. Slow pressure gradient. However, in most cases, a subaortic pressure
titration of the epidural is important. The sympathectomy- gradient is present and the ventricle is less compliant. This leads
induced reduction of afterload following neuraxial anesthesia is to a reduction in passive ventricular filling during diastole. Atrial
potentially beneficial provided BP is maintained.108 Intrathecal contraction becomes an important factor in increasing LVEDV.
opioids via a CSE or continuous spinal technique are an option for Factors that impact on the degree of obstruction include
labor analgesia. LVEDV, force of ventricular contraction, and transmural pressure
If the patient is able to tolerate the supine left-tilt position, an that distends the outflow tract. Inotropic agents or conditions
epidural anesthetic for C/S is probably the best option. A continu- that increase myocardial contractility and SVR will worsen the
ous spinal anesthetic has been used successfully in a patient outflow obstruction. Conditions that decrease preload will also
with severe PPCM;109 however, a single-shot spinal technique worsen obstruction by decreasing LV volume. When the LV out-
is not recommended because the subsequent rapid hemody- flow tract is narrowed, CO falls and MR may occur since the mitral
namic changes may not be well tolerated. Epidural anesthesia valve becomes the point of relief for the build up of ventricular
with noninvasive hemodynamic monitoring has been reported pressure.
for C/S.107 In pregnancy, the decrease in SVR along with an increase in
If GA is necessary, a ˜˜cardiac™™ induction technique with a HR and contractility are physiologically deleterious to this con-
cardio-stable induction agent (e.g. etomidate) and high doses of dition. Conversely, an increase in intravascular volume allows
opioid are recommended. In one case report, a patient with for a larger ventricular volume and decreases outflow obstruc-
undiagnosed cardiomyopathy suffered a cardiac arrest at induc- tion. A decrease in preload associated with aortocaval compres-
tion of GA for emergency C/S.110 Fortunately, the mother and sion in the third trimester and the Valsalva maneuver during
baby were successfully resuscitated. delivery can increase outflow obstruction. Usually, the physio-
There is no consensus on the possibility of subsequent preg- logical changes of pregnancy are well tolerated in patients with
nancies in survivors of PPCM.13,84 In patients not recovering HOCM.114 However, latent HOCM may become a clinical pro-
ventricular function and in heart failure, future pregnancies are blem and sudden death from HOCM has been reported in
pregnancy.115,116
not recommended. Even in women who have recovered clini-
cally, 20% will deteriorate in subsequent pregnancies. In a
woman with previous PPCM and normal ventricular function at
Management principles
rest, systolic dysfunction can be unmasked using dobutamine
echocardiography.111 Failure to tolerate this stress test may indi-  Where appropriate, use invasive monitoring in symptomatic
cate that the patient will not be able to tolerate a future preg- patients or patients with atrial dysrhythmias.
 Avoid decreases in preload. Increased blood volume and main-
nancy. Echocardiographic evidence of LV dysfunction includes
fractional shortening <20% and LV end diastolic dimension tenance of venous return is important in order to minimize
>6 cm.112 Recurrence of PPCM is possible and mortality asso- outflow obstruction.
ciated with a recurrence is even higher.113  Maintain a normal to slow HR and aggressively treat any atrial
dysrhythmias. Tachycardia limits diastolic filling, which
decreases LVEDV and increases contractility, which, in turn,
Hypertrophic obstructive cardiomyopathy
will increase LV outflow tract obstruction.
 Avoid increases in contractility as this increases the dynamic
Hypertrophic obstructive cardiomyopathy (HOCM) or idiopathic
hypertrophic subvalvular stenosis (IHSS) is a disease that is char- obstruction and may reduce CO. Beta-blockade is useful in
acterized by a dynamic LV outflow tract obstruction, caused by patients with HOCM to treat LV outflow obstruction by reducing
a contracting hypertrophied ventricle and septum during systole. cardiac contractility and HR. However, there is concern that
This disease usually affects patients in their 20s to 30s and is beta-blocker therapy during pregnancy might cause fetal brady-
occasionally seen in pregnancy. Most patients have a fairly cardia and intrauterine growth restriction (IUGR). The use of
benign course, but patients with HOCM are at increased risk for esmolol is controversial and there have been reports of hypoto-
dysrhythmias and sudden death. Affected patients may be nia, hypotension, hypoglycemia, and bradycardia in a neonate
born to a parturient with HOCM treated with esmolol.115,117
asymptomatic or have mild symptoms (palpitations, dyspnea



12
Chapter 1


Heart transplant recipients
Labetalol in 0.25 mg/kg increments up to 1 mg/kg may be
preferable.
(see Chapter 22)
 Avoid sudden decreases in SVR. Maintenance of SVR will
decrease outflow obstruction.
Aortic dissection
 Treat hypotension with an alpha-agonist (e.g. phenylephrine or
metaraminol). Try to avoid ephedrine as it may increase the There is an association between pregnancy and aortic dissection,
dynamic obstruction. and 50% of all dissections in women under 40 years old occur
during pregnancy.125,126 Maternal mortality is very high, but is
similar to the nonpregnant state. Although aortic dissection is
Anesthetic options
rare, it is an important cause of maternal mortality.3,4,66 Possible
Vaginal delivery is considered safe, although attempts should etiological factors of aortic dissection during pregnancy include
be made to minimize the period of ˜˜bearing down™™ during the connective tissue disease (in particular, Marfan syndrome),
second stage of labor. Regional anesthesia has been used success- severe preeclampsia, sepsis, atherosclerosis, and coarctation of
fully in laboring patients with HOCM despite concerns about the aorta (see Chapter 3). The diagnosis should be suspected in
associated afterload reduction.115,118 Appropriate prehydration, anyone with abdominal, thoracic, or interscapular pain; however,
monitoring, and the use of drugs like phenylephrine or metara- painless dissection is common with Marfan syndrome. There
minol to maintain SVR are important. Both conventional epi- is cardiovascular involvement in 80% of patients with Marfan
dural119 and CSE120 have been used in this setting to provide syndrome.3 Presentation depends on the extent and location of
labor analgesia. In one case report, continuous spinal analgesia the dissection with 70% affecting the ascending aorta.73 Diagnosis
with an opioid as the sole intrathecal agent provided excellent is made by computed tomography (CT) scan or TEE.
pain relief and hemodynamic stability.118 The intrathecal opioid
allowed rapid analgesic onset without the sympathetic block and
afterload reduction.118,120 Epidural and continuous spinal analge- Management principles
sia attenuate increases in HR and contractility from endogenous
Nonemergent situation: The decision to repair the aorta should be
catecholamines (pain and anxiety) during labor. Expulsive efforts
based on the patient™s condition and gestational age of the fetus.
and Valsalva maneuvers can be reduced by effective epidural
The risk of dissection increases with the duration of pregnancy
analgesia. Ephedrine is contraindicated in the treatment of hypo-
and the diameter of the ascending aorta. In a case series of
tension associated with HOCM due to the risk of tachycardia,
pregnant women with acute aortic dissection, most dissections
therefore phenylephrine (50 mg increments) is the treatment of
happened in the third trimester.127 The ascending aorta at time
choice for hypotension following sympathetic blockade.
of dissection was 4.8 cm. Aortic diameters over 4 cm are generally
Ropivacaine has theoretical advantages over bupivacaine in that
considered critical. Monthly ultrasound inspections of the aorta
it is less cardiotoxic. However, low concentrations of bupivacaine
are recommended to detect possible early rupture. Premature
can be used safely in these patients.
delivery via C/S or induction of labor is recommended when the
Spinal and epidural anesthesia for C/S cause a reduction in pre-
aortic root diameter is greater than 4.5 cm.13,127 Management
load and afterload, which has a potential adverse impact in
should be individualized and based on a multidisciplinary team
patients with HOCM.119,121 The successful use of GA for C/S has
reviewing the patient™s condition throughout pregnancy. Before
been described in women with HOCM.122 Although volatile anes-
fetal viability, aortic repair with a fetus in situ is justified given
thetic agents are beneficial in that they produce a reduction in
the high mortality of nonoperative treatment.128,129 If the fetus is
myocardial contractility they should be used cautiously to avoid
viable, primary C/S or vaginal delivery with concomitant or
a marked fall in SVR. While GA is traditionally recommended for
staged surgical repair is indicated.125
these patients, carefully titrated epidural anesthesia has been used
Emergent situation: In the case of acute rupture or hemodynamic
successfully for C/S.123 A single-shot spinal anesthetic is not
deterioration, expedited surgery and resuscitation may be
recommended because of the rapid onset of sympathetic block-
necessary. Cesarean section should be performed once control
ade. Subarachnoid anesthesia for an orthopedic procedure in a
of the aortic dissection is achieved.
patient with HOCM resulted in an increased left ventriculo-aortic
gradient, and concomitant deterioration in coronary perfusion.121
The critical determinants of a good outcome are careful titra-
Anesthetic options
tion of anesthetic agents, adequate volume loading, and prompt
replacement of blood loss guided by invasive hemodynamic Regional anesthesia is recommended for labor pain as it can
monitoring. Although the tachycardia and hypotension asso- effectively reduce sheer wall stress and wall tension associated
with pain during labor and delivery.66 Vaginal delivery under
ciated with oxytocin are problematic in women with HOCM, a
dilute oxytocin infusion will likely be well tolerated.122 regional anesthesia has been described in patients with Marfan
syndrome and aortic dissection.130 The BP should be kept normal
Postpartum pulmonary edema in parturients with IHSS has
been reported.124 Patients should be closely monitored for wor- or slightly below normal. All antihypertensive medication should
sening outflow obstruction resulting from the diuresis that occurs be continued peripartum. Beta-blockers can be titrated to control
the BP during labor and delivery.66 Preparations should be made
in the first 48“72 hours postpartum.



13
1 Cardiovascular and respiratory disorders


for possible rupture with large-bore i.v. access, blood and resus- maternal and fetal mortality ranges from 21“37% and 12“34%
respectively.140,141 Maternal mortality is greatest (approximately
citation equipment available.
The best anesthetic method for C/S is controversial. General 45%) if the MI is late in pregnancy, or when delivery occurs within
14 days of the initial infarction.140,141
anesthesia is associated with a hypertensive response to intuba-
tion and surgical stimulation that may promote rupture or dis-
section progress. Efforts should be made to prevent increases in
Pathophysiology
BP and to reduce the cardiovascular response to endotracheal
intubation. General anesthesia may be necessary in the antico- Myocardial ischemia occurs when oxygen demand outstrips oxy-
agulated patient or in the emergent situation. In Marfan syn- gen supply. In MI during pregnancy, atherosclerosis is found to
be the cause in less than half the cases.140 The coronary arteries
drome, regional anesthesia can be associated with marked
often appear normal at angiography140,142 and other suggested
hypotension and increased risk of epidural hematoma due to
epidural vein fragility. causes include coronary spasm, arteritis (e.g. Kawasaki Disease “
Chapter 3 ), or in situ thrombosis.
Normal pregnancy is accompanied by increases in HR, myo-
Cardiopulmonary bypass during pregnancy
cardial wall tension, basal metabolic rate, and oxygen consump-
The first extracorporeal circulation or cardiopulmonary bypass tion. Labor and delivery lead to further increases in oxygen
(CPB) during pregnancy to facilitate open-heart surgery was consumption and demand, which may seriously compromise
described by Leyse et al.131 in a woman at 18 weeks™ gestation women with ischemic heart disease (IHD). The increase in oxy-
with congenital AS. Cardiopulmonary bypass has been necessary gen consumption peaks at the time of delivery, and remains
during pregnancy and in the peripartum period to facilitate open- elevated in the immediate postpartum period. Even asympto-
valve surgery and to manage individual cases of aortic dissection, matic patients with coronary artery disease during pregnancy
massive pulmonary embolus, amniotic fluid embolus, and cor- are at risk of ischemia or infarction during the peripartum and
onary artery dissection. If possible, surgery requiring CPB should postpartum periods.
be delayed until the second trimester, or later. If the parturient Most cases of peripartum MI are in patients without a history of
tolerates pregnancy, a primary C/S with concomitant or staged IHD. Characteristic symptoms, ECG changes and serial elevated
CPB with surgical repair can be performed.132 cardiac enzymes diagnostic of MI in nonpregnant patients, are
less reliable during pregnancy.66 Signs and symptoms of myocar-
Most cardiac operations with CPB during pregnancy can be per-
formed with reasonable safety in the mother, but there is increased dial ischemia in pregnancy can be similar to normal signs and
risk for the fetus.133,134 The well-being of the mother and fetus must symptoms of pregnancy. These include poor exercise tolerance,
be considered although the best interests of the two may not always shortness of breath, diaphoresis, and chest pain. In normal preg-
coincide and optimal therapy may be a compromise.135 nancy the ECG may show left-axis deviation and reversible ST-,
During CPB in pregnancy, high pump flows (30“50% increase T-, and Q-wave changes. ST-segment depression is common
over the nonpregnant state) should be maintained. Perfusion during C/S under regional anesthesia without evidence of myo-
cardial ischemia.143 If an MI during pregnancy is suspected, diag-
pressures >60 mmHg appear optimal to maintain utero-placental
perfusion.1 One report describes the successful treatment of nosis can be confirmed by measuring cardiac specific troponin I
fetal bradycardia during CPB by increasing the perfusion rate.136 levels >0.15 ng/ml. Creatine kinase levels may not be helpful
since they increase during normal labor.144
Hypothermia can reduce utero-placental perfusion and cause fetal
hypoxia.3 Temperatures <328C have the potential to cause fetal An exercise stress ECG or echocardiography with inducible ische-
dysrhythmias and cardiac arrest. Continuous intraoperative fetal mia helps to confirm the diagnosis of IHD. Recommendations
monitoring is important during CPB in order to detect fetal dys- for stress testing during pregnancy should follow the ACC and the
AHA guidelines.145 Heavy exercise during pregnancy may decrease
rhythmias and bradycardia.
Another problem associated with CPB during pregnancy is uterine blood flow, and testing should be done with fetal moni-
toring and an exercise goal limited to 70% maximum HR.146
severe postpartum hemorrhage. This was described during an
emergency mitral valve replacement immediately after C/S.137 Echocardiography is safe in pregnancy; however, the safety of
Aprotinin, a protease inhibitor, has been used to effectively treat pharmacologic stress-testing echocardiography is unknown.
a similar problem in an obstetric patient following CPB.138
Patients requiring CPB should be managed in a tertiary center
Management principles
with multidisciplinary team involvement.135
 Efforts should be made to limit myocardial oxygen demand
and maximize supply throughout pregnancy and during
Peripartum ischemic heart disease
parturition. Myocardial ischemia occurs when oxygen demand
Acute myocardial infarction (MI) in pregnancy is relatively rare outstrips oxygen supply.
with a reported incidence of 1 in 10 000.139 However, the inci-  Anemia should be treated and hematocrit maintained
dence can be expected to increase due to advancing maternal age, above 30%.
tobacco, and cocaine abuse.1,140 Peripartum MI carries substan-  Medical management of IHD includes optimal positioning to
tial maternal and fetal morbidity and mortality.140,141 Overall avoid aortocaval compression, oxygen administration, aspirin,



14
Chapter 1


beta-blockers, nitroglycerin infusion, calcium channel block- Consider light sedation (e.g. midazolam i.v. 0.5“1 mg) to minimize
ers, and anticoagulation. Aspirin is considered safe at doses anxiety and pain during line and epidural placement. Shivering
<150 mg per day, especially during the second and third trime- increases oxygen consumption and must be treated aggressively
ster.22 Although there are no reports of teratogenicity with (e.g. meperidine i.v. 12.5“25 mg). Avoid shivering by using fluid
beta-blockers, there have been reports of intrauterine growth warmers, forced air warmers, and increasing the operating room
restriction (IUGR), fetal bradycardia, hypoglycemia, and temperature. Phenylephrine is the drug of choice to treat hypoten-
hyperbilirubinemia at birth with both propranolol and esmolol sion and minimize an increase in HR. Preventing an increase in HR
therapy. Selective beta-blockers are probably safer with fewer is critical because tachycardia increases myocardial demand and
fetal complications reported. Nitroglycerin infusion and cal- reduces oxygen supply (shorter diastolic coronary perfusion time).
cium channel blockers may have tocolytic effects and therefore If GA is necessary for obstetric indications, then a high dose opioid
may increase the risk of uterine atony. Angiotensin-converting technique is recommended to reduce the cardiovascular response
enzyme inhibitors and statins are contraindicated in preg- to endotracheal intubation and surgery.
nancy and should be avoided. Continuous postpartum monitoring is essential. Patients
 There are a number of successful reports of percutaneous should be managed by a multidisciplinary team for optimal out-
coronary angioplasty following MI in pregnancy.147,148,149 come. Specialist advice is necessary if these patients are contem-
However, there are no reports of this revascularization option plating future pregnancies, and future cardiac risk will depend
upon post-MI cardiac function.155
in pregnant patients with stable coronary artery disease.
 Successful coronary artery bypass grafting during pregnancy
has been reported.150 Although the risk of CPB during preg- Congenital heart disease in the pregnant patient
nancy is similar to that of nonpregnant patients (3% overall),
General principles
the fetal mortality remains high at 19%.150
 Thrombolytic agent (e.g. streptokinase, tissue plasminogen acti- In developed countries, pregnant women with CHD outnumber
vator) administration to pregnant women has been reported in those with rheumatic heart disease.13,156 With improvements in
the literature.140,151,152 However, the potential risks of maternal surgical and medical management, an increasing number of
and fetal hemorrhage may outweigh the benefits. patients with corrected or partially corrected CHD are surviving
 Although experience is limited, percutaneous coronary angio- to childbearing age and presenting for labor and delivery. The
plasty Æ stenting may be the treatment of choice in pregnant outcome of a pregnant woman with CHD is related to her NYHA
patients with MI. functional status, the type of lesion, and the nature of prior
palliative or corrective surgery. In particular, patients with severe
LV outflow tract obstruction, pulmonary hypertension, or cyano-
Anesthetic options
tic heart disease are at greater risk from pregnancy.13
Patients should be managed in a setting where continuous ECG The anesthetic management of obstetric patients with CHD is
monitoring can occur. If possible, delivery should be postponed challenging and there is a lack of evidence-based literature to
at least two weeks after an MI.140,153 Cautious use of oxytocin is guide management due to the rarity and heterogeneity of lesions.
important to avoid hypotension.154 Ergot alkaloids (e.g. mether- Furthermore, the anesthetic approach toward two parturients
gine) may cause coronary spasm and should be avoided.3 with the same CHD lesion may differ significantly depending on
Prostaglandin F2-alpha (hemabate) should also be used with the severity of the lesion (i.e. minimal end-organ cardiopulmon-
caution as it may cause hypertension in the systemic and pul- ary effect versus end-stage Eisenmenger syndrome (ES) versus
monary circulations. postpalliation versus postcomplete repair).157,158 Regardless of
It is important to provide optimal pain relief during labor in order the CHD lesion, the strategy should be to identify the cardiopul-
to minimize the cardiovascular stress of labor and delivery. This monary pathophysiology (primary and secondary), and manage
can be achieved by a slow controlled induction of epidural analge- it within the context of the physiologic changes of pregnancy. Any
sia. If patients are anticoagulated, follow ASRA guidelines (see parturient with a significant CHD lesion should be managed in
Table 1.7) prior to inducing a neuraxial block. There are advantages conjunction with a cardiologist at a tertiary care facility.157,159 As
and disadvantages of vaginal and C/S with no convincing evidence the infant is also at risk of CHD (2“16%),160 these infants may
that either option is superior32 (see Table 1.8). Some authors prefer require specialized care.77,158
vaginal delivery if obstetrically indicated.141 However, limits to the Patients with CHD lesions should receive bacterial endocar-
duration of labor should be discussed and preparations for a poten- ditis prophylaxis Æ thomboprophylaxis (see Tables 1.5 and 1.6).
tial C/S considered. The use of forceps or vacuum to assist delivery Meticulous care is required in patients with CHD shunt lesions to
and minimize prolonged pushing is preferable. ensure all peripheral and central i.v. lines are free of air bubbles.
A regional anesthetic technique is appropriate for C/S provided
preload is maintained and reflex tachycardia is avoided. Afterload
Monitoring
reduction associated with regional anesthesia is beneficial in
decreasing cardiac demand. Slowly titrated epidural anesthesia Patients with CHD require special considerations when planning
monitoring needs.161 Arterial lines may need to be placed on the
is ideal to prevent abrupt fluctuations in preload and afterload.
A single-shot spinal technique is relatively contraindicated. opposite side of the previous shunt (e.g. Blalock-Tausig shunt).

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