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much better prognosis than acute AR.16 In women of
BOX 51.1 SELECTION OFNEURAXIAL ANESTHETIC
TECHNIQUE
• Combined Spinal- Epidural technique
• Optimal technique
• Intrathecal opioids during stage I(excellent analgesia
without sympatheticblock)
• 15– 25 ugs fentanyl + 0.25– 0.5 mg morphine
(preservative- free)
• Dilute local anesthetics for late 1st stage and second
stage oflabor
childbearing age, etiologies of AR include congenital
bicuspid aortic valve disease, history of rheumatic heart
disease or infective endocarditis, aortic annular dilation,
and rarely antiphospholipid syndrome.
4,8,17,18
Aortic
regurgitation imparts a lower pregnancy risk than its stenotic counterpart, since the physiologic increase in heart
rate and decrease in SVR typical in pregnancy match
hemodynamic goalsofAR.
Antepartum evaluation includes assessment of functional status and symptoms. Aortic regurgitation is classied as mild if the regurgitant volume is less than 20% of the
• 0.625%– 0.125% bupivacaine + fentanyl 2– 2.5ugs/ mL
• Epidural with dilute local anesthetics
• 0.625%– 0.1.25% bupivacaine + fentanyl
2– 2.5ugs/mL
• ugs/ mL:micrograms per milliliter
total le ventricular stroke volume, moderate if between
20% and 39%, moderately severe if between 40% and
60%, and severe if greater than 60%.
16,19,20
Asymptomatic
women with mild to moderate AR and preserved LV function are at low risk for cardiovascular complications such as
arrhythmias. Maternal risk for heart failure is heightened in
symptomatic women with severe AR and compromised LV
function. ese patients should preferably undergo surgical
opioid followed by infusion of low- dose local anesthetic/ opioid solutions can also be used. ese techniques allow for
incremental extension to surgical anesthesia should operative
vaginal or cesarean delivery become necessary; furthermore,
such techniques may also allow use of neuraxial morphine
for postoperative pain control. Single- shot spinal anesthesia
valve repair prior to pregnancy. erapy for symptomatic
pregnant women with AR includes diuretics, beta blockers,
and/ or vasodilators to relieve symptoms of pulmonary congestion. Surgical intervention for correction of regurgitant
lesions is rarely warranted during pregnancy except in the
most severecases.
is contraindicated in patients with AS because their restricted
capacity to increase cardiac output makes them unable to
compensate for the eects of sympathectomy.
In cases of severely symptomatic AS, general endotracheal anesthesia for cesarean delivery may be the most
appropriate choice. Induction and intubation goals include
rapid tracheal intubation to avoid risk of aspiration while
also limiting unfavorable hemodynamic responses such as
excessive myocardial depression, vasodilation, and tachycardia. General anesthesia also allows the use of continuous
intraoperative TEE. With all modes of delivery and anesthetic technique, le uterine displacement must be maintained and uids judiciously administered to maintain the
aforementioned hemodynamic goals. e use of oxytocin
should be carefully considered and administered in lowdose infusion to avoid hypotension.
6
7
Anesthesia forLabor and Delivery inParturients
withAortic Regurgitation
Vaginal delivery with a shortened and oen assisted second stage of labor is the preferred mode of delivery in these
patients, especially if concurrent aortic dilation is present.
Anesthetic management principles for AR include the
following: (1) avoidance of aortocaval compression, (ii)
avoidance of bradycardia and maintenance of heart rate
between 80 and 100 beats per minute, (iii) avoidance of
myocardial depression, and (iv) avoidance of increase in
SVR (Table 51.1). With appropriate hemodynamic monitoring, both general and neuraxial anesthesia may be safely
performed in pregnant patients with all severities of AR.
Acarefully titrated neuraxial technique may be preferred,
AORTIC REGURGITATION
Aortic regurgitation (AR) refers to incompetency and/
or disturbance of the aortic valve that results in the backward flow of blood from the aorta into the LV during
diastole. Chronic AR is more prevalent and carries a
as it provides the benets of decreasing aerload, preventing increased SVR, and minimizing risk of le ventricular
volume overload, while facilitating an assisted second stage.
e indirect- acting sympathomimetic, ephedrine, is the
rst- line vasopressor used in AR; however, phenylephrine
may be administered in small aliquots.
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MITRAL STENOSIS
Rheumatic mitral valve stenosis is the most common
acquired heart disease in the pregnant population worldwide. Mitral stenosis (MS) is classied as mild (valve area
1.5– 2.0cm2), moderate (valve area 1.0– 1.5cm2), or severe
(valve area <1.0 cm2). In severe MS, an underlled LV
success rate was 98%.23 Surgical commissurotomy has a
lower maternal mortality rate, but is associated with high
fetal mortality rates.24 Surgical mitral valve replacement is
reserved only for those patients who have symptoms refractory to medical therapy in whom valvuloplasty is contraindicated and surgical commissurotomy is not appropriate.
25
leads to a xed cardiac output state. Eventually this causes
elevated le atrial pressures, pulmonary hypertension, and
pulmonary edema. Patients are at highest risk for pulmonary edema near the end of the second trimester/ start of
third trimester, when the intravascular volume is highest.
Compensatory right ventricular (RV) hypertrophy leads
to right heart failure if MS persists untreated. Radiologic
studies may be normal with mild MS and typically reveal
le atrial and right ventricular enlargement and even pulmonary edema as the disease progresses. Electrocardiogram
changes include broad P waves in lead V1, signifying le
atrial enlargement, and right axis deviation signifying right
atrial enlargement.
21
Parturients with MS oen become symptomatic because
of the physiologic increases in plasma volume and cardiac
output. Initial symptoms include fatigue and dyspnea
on exertion followed by paroxysmal nocturnal dyspnea,
orthopnea, and dyspnea at rest. Complications in parturients with MS include atrial tachyarrhythmias related to le
atrial dilation, pulmonary edema, thromboembolic events,
and potentially hemodynamic collapse. Hemoptysis with
rupture of bronchopulmonary varices can also occur. ere
is also a signicant risk for premature birth and intrauterine
growth restriction. In one study of parturients with severe
MS, 67% developed a maternal cardiac event, and 44% of
infants were born prematurely or died.
22
Pregnancy outcome depends on the severity of the MS,
presence of atrial dilatation and arrhythmia, and severity of
pulmonary hypertension.
As with other valvular lesions, preconception counseling is important in patients with known severe MS. Patients
with a mitral orice area > 1.5cm2 can usually be treated
medically, whereas more advanced MS oen requires intervention, ideally prior to pregnancy. Closed mitral balloon
valvuloplasty, open surgical commissurotomy, or open
heart valve replacement are considered depending on clinical scenario. Given the risk of surgery to both mother and
fetus, closed percutaneous mitral valvuloplasty is preferred
for pregnant patients with rheumatic MS, despite a known
high incidence of restenosis requiring surgical intervention
in the future. In one study of such cases, maternal mortality rate for percutaneous mitral valvuloplasty was 0.2%
and fetal mortality rate was 2%; overall, the procedural
Anesthesia forLabor and Delivery inParturients
withMitral Stenosis
Most reports recommend vaginal delivery under epidural
anesthesia, unless there is an obstetric reason for cesarean
delivery. In a study by Goldszmidt and others, only 29%–
31% of the 522 women with heart disease required cesarean
delivery, and nearly 70% of them underwent vaginal delivery with epidural analgesia.
26
During labor, management goals include preventing
elevated sympathetic outow secondary to labor pain that
can worsen ow across the mitral valve, leading to acute
atrial arrhythmia and/ or pulmonary edema. Tachycardia
should be avoided and normal sinus rhythm maintained.
Early neuraxial analgesia is a critical part of management,
as is heart rate control with beta blockade and cardioversion if needed. Some practitioners prefer combined- spinal
epidural labor analgesia with a lipophilic narcotic and ultralow concentration infusion of bupivacaine. Continuous
telemetry, pulse oximetry, and prn oxygen supplementation
are recommended for all laboring parturients, and providers should have a low threshold to initiate invasive arterial blood pressure monitoring, especially in patients with
severe MS or pulmonary hypertension.
Phenylephrine is the vasopressor of choice to manage hypotension. Epinephrine- containing epidural solutions should be used with caution because of the potential
for accidental intravascular injection. Terbutaline should
be avoided if uterine tocolysis is required. Avoidance
of Valsalva maneuver with assisted second stage may be
required depending on the severity of the MS. Epidural
analgesia again allows for titration to surgical anesthesia, should this be necessary, while also increasing venous
capacitance to accommodate the postdelivery autotransfusion and minimize right heart strain.
If cesarean delivery is required, gradual titration of an
epidural block with continuous infusion of local anesthetic
can oen be performed, however some NYHA ClassIII
and IV patients may be better managed under general
anesthesia, as numerous case reports demonstrate positive
fetal and maternal outcomes. If general anesthesia is used,
narcotics, beta blockade, and IV lidocaine should be used
VALVULAR DISEASE 367
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to minimize hemodynamic response to laryngoscopy and
intubation. In patients with severe MS, especially if symptomatic, invasive monitoring prior to induction of anesthesia should be considered.
MITRAL REGURGITATION
Mitral valve insuciency or regurgitation (MR) is the second most common valvular disease observed in pregnancy.
Even in 28% of “normal” pregnancies, there is oen some
degree of mitral insuciency.27 e most common etiology of MR is myxomatous disease or mitral valve prolapse.
Diagnosis may initially be clinical, as the chief sign is a
pansystolic murmur at the cardiac apex, referred to the le
TABLE51.2 COMPARISON OFINTRATHECAL NARCOTICS
VERSUS EPIDURAL DILUTE LOCAL ANESTHETIC FOREARLY
EPIDURAL INPARTURIENTS WITHCARDIAC LESIONS
Intrathecal Narcotic Epidural Local Anesthetic Solutions
• Quick onset
• Selective analgesia
• No sympatheticblock
• No motor block
SOURCE:Reprinted with permission from Chandrasekhar S, Suresh MS.
Chapter45:Anesthetic management of critically ill parturient with cardiac disease.
In:Belfort M, Saade GR, etal., eds., Critical Care Obstetrics. 5th ed. NewYork:Blackwell-
Wiley; 2010:639– 55.
• Unlimited duration analgesia (catheter)
• Titratability ofblock
• Relative hemodynamic stability
• Ability to use different local anesthetics/
• different situation
• 1st stagelabor
• 2nd stagelabor
• c/ section
axilla or infrascapular area. Electrocardiogram may be normal if mild, but can show LVH or RVH if severe. Similarly,
chest radiograph reveals le ventricular enlargement.
Echocardiography is indicated in all suspected cases of
mitral valve insuciency to conrm its presence and determine its severity. e principal symptoms of advanced MR
are those of le ventricular failure. Atrial brillation occurs
in approximately one- third of patients, and late sequelae
include pulmonary congestion, pulmonary hypertension,
and right ventricular enlargement. Once patients demonstrate heart failure symptoms, deterioration occurs rapidly,
with a 5- year mortality of50%.
Mitral valve regurgitation, even when severe, is usually very well tolerated in pregnancy. Increased LV volume
is typically oset by a decrease in vascular resistance and
increased cardiac output. However, patients with LV dys-
still encouraged, and most patients tolerate vaginal delivery
with good outcomes.
Patients with severe MR and symptoms of LV failure will need strict uid management and oen require
diuretics and aerload reduction during or aer delivery.
e angiotensin converting enzyme (ACE) inhibitors are
contraindicated in pregnancy; thus nitrates and calcium
channel blockers are rst- line agents. Invasive hemodynamic monitoring may be needed in patients with severe
LV dysfunction.
e principles of anesthetic management during cesarean are the same as for vaginal delivery:tolerance of a higher
heart rate (sinus rhythm), lower systemic vascular resistance,
and avoidance of myocardial depression (Table51.2).
function, moderate pulmonary hypertension, or NYHA
functional classes III- IV remain at increased risk for heart
failure and arrhythmias. In these patients maternal mortality may be as high as 7%.28 Parturients with symptoms of
LV dilation or cardiomyopathy may require activity limitations, as well as medical therapy with diuretics and aerload
reduction. Antiarrhythmics may be necessary with signicant le atrial enlargement, and severely decreased systolic
function should be treated with inotropes.
TRICUSPID REGURGITATION AND TRICUSPID
STENOSIS
Tricuspid regurgitation (TR) and tricuspid stenosis (TS)
are rarely encountered as isolated lesions in pregnancy.
When present as the primary valvular lesion, TR is usually
benign and is not associated with any signicant clinical
diculty or functional impairment. Its presence may be discovered coincidentally during investigation of the etiology
Anesthesia forVaginal and Cesarean Delivery
inParturients withMitral Regurgitation
Vaginal delivery is preferred and cesarean delivery
reserved for obstetric indications. Asymptomatic patients
with unchanged echocardiographic evaluation may be
approached in a routine but cautious fashion. Standard
monitoring is likely to be sucient. Early epidural placement to prevent increases in SVR from pain and anxiety is
of new- onset murmur in pregnancy.29 Overall, perioperative
hemodynamic management of TR should aim to (1)avoid
aortocaval compression, (2)augment right ventricular preload, (3)maintain normal to high heart rates, (4)maintain
contractility, (5)maintain systemic vascular resistance, and
(6)decrease pulmonary vascular resistance.
19
Tricuspid stenosis is most frequently associated with
rheumatic MS when it is encountered in pregnancy. Other
etiologies of TS include systemic lupus erythematosus,
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369
endomyocardial broelastosis, and carcinoid syndrome.19
Aected parturients may experience symptoms of rightsided heart failure.21 e goals of hemodynamic management should be to (1) avoid aortocaval compression,
(2)maintain or slightly increase right ventricular preload,
(3)maintain normal sinus rhythm, (4) maintain contractility, (5) maintain contractility as this helps to ensure
adequate cardiac output, (6) increase systemic vascular
resistance, and (7)maintain pulmonary vascular resistance
in the normal range.13 Importantly, anesthetic management
of parturients with tricuspid disease also requires consideration of the hemodynamic goals of any coinciding lesions,
as they may be signicant contributors to the patient’s
symptomatology and clinical course.
assessment and ongoing evaluation that is best achieved
via a multidisciplinary approach.
• Valvular lesions representative of mixed pathophysiology
are more commonly encountered than pure lesions.
Anesthesiologists must decipher which lesion is
most hemodynamically signicant and determine
what takes precedence when determining optimal
managementgoals.
• Invasive hemodynamic monitoring should be used
where appropriate.
• Anesthetic technique should be adapted to optimally
meet the demands of the parturient’s disease.
• e peripartum period should be managed carefully
ANTICOAGULATION THERAPY INA
PARTURIENT WITHCARDIAC DISEASE
e indications for anticoagulation in a pregnant cardiac
patient with valvulopathy are mechanical heart valves, new-
as it poses risks due to hemodynamic changes and
sympathetic surges.
• e autotransfusion aer delivery must be anticipated.
• Judicious uid and oxytocin management should be
provided.
onset atrial brillation, dilated cardiomyopathy, and cardiopulmonary bypass surgery.
Oral anticoagulation with warfarin has been associated
with the lowest maternal mortality and rate of thromboem-
CASE- BASED LEARNING DISCUSSION
bolism during pregnancy. However, it is well known that
warfarin’s use in the rst trimester can cause fetal growth
restriction, spontaneous abortion, embryopathy, premature birth, and fetal and placental hemorrhage in the third
trimester.
Unfractionated heparin and low molecular weight heparin (LMWH) do not cross the placenta and are thought
to have no fetal teratogenic eects. However, these drugs
may not be as eective as warfarin in preventing thrombosis. Clinicians typically use heparin in the rst trimester of
pregnancy, switch to warfarin or enoxaparin until 35– 36
weeks of gestation, and then restart heparin until delivery.
A special concern in the anesthetic management of anticoagulated patients is the risk of epidural or spinal hematoma
development during neuraxial anesthesia. e American
1. How are patients with MS evaluated? What do
obstetricians consider when creating a delivery plan?
What are the hemodynamic goals for the patient?
How can you optimize your anesthetic plan to account
for these goals? What do you anticipate will happen
following delivery? Do you want invasive monitoring
for this patient?
2. What is the most common cause of MR in pregnant
patients? What types of symptoms do patients with
MR typically present with? Should this patient have a
scheduled elective cesarean delivery due to her valvular
disease? What if she also had moderate concurrent AR?
What is the vasopressor of choice forMR?
Society for Regional Anesthesia (ASRA) has provided specic clinician guidelines regarding placement and removal
of neuraxial blocks in patients on anticoagulation.
30
REFERENCES
FOLLOW- UP/ KEYPOINTS
• Management of the parturient with valvular disease
presents unique challenges. It requires thorough
VALVULAR DISEASE 369
1. Small MJ, James AH, Kershaw T, ames B, Gunatilake R, Brown
H. Near- miss maternal mortality:cardiac dysfunction as the principal cause of obstetric intensive care unit admissions. Obstetrics and
Gynecology. 2012;119(2 Pt 1):250– 5.
2. Lewis G. Saving mothers’ lives:the continuing benets for maternal
health from the United Kingdom (UK) condential enquires into
maternal deaths. Semin Perinatol. 2012;36(1):19– 26.
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3. Creanga A, Berg C, Sylverson C, Seed K, Bruce FC, Callaghan
W. Pregnancy- related mortality in the United States, 2006– 2010.
Obstetrics and Gynecology. 2015;125(1):5– 12.
4. Nanna M, Stergiopoulos K. Pregnancy complicated by valvular
heart disease:an update. J Am Heart Assoc. 2014;3(3):e000712.
5. Kaemmerer HHJ. Congenital heart disease:transition from adolescence to adulthood. Internist (Berl). 2009;50:1221– 2,1224– 7.
6. Chandrasekhar S, Cook CR, Collard CD. Cardiac surgery in the
parturient. Anesth Analg. 2009;108(3):777– 85.
7. Chandrasekhar S, Suresh MS. Chapter45:Anesthetic management
of critically ill parturient with cardiac disease. In:Belfort M, Saade
GR, etal., eds., Critical Care Obstetrics. 5th ed. NewYork:BlackwellWiley; 2010:639– 55.
8. Regitz- Zagrosek V, Lundqvist CB, Borghi C, etal. ESC Guidelines
on the management of cardiovascular diseases during pregnancy.
European Heart Journal. 2011;32:3147– 97.
9. Lyons G. Saving mothers’ lives:condential enquiry into maternal
and child health 2003- 5. Int J Obstet Anesth. 2008;17(2):103– 5.
10. Bonow RO, Carabello BA, Chatterjee K, et al. 2008 Focused
update incorporated into the ACC/ AHA 2006 guidelines for the
management of patients with valvular heart disease: a report of
the American College of Cardiology/ American Heart Association
Task Force on Practice Guidelines (Writing Committee to Revise
the 1998 Guidelines for the Management of Patients With
Valvular Heart Disease):endorsed by the Society of Cardiovascular
Anesthesiologists, Society for Cardiovascular Angiography and
Interventions, and Society of oracic Surgeons. Circulation.
2008;118(15):e523– 661.
11. Yap SC, Drenthen W, Pieper PG, etal. Risk of complications during
pregnancy in women with congenital aortic stenosis. Int J Cardiol.
2008;126(2):240– 6.
12. Vahanian A, Baumgartner H, Bax J, etal. Guidelines on the management of valvular heart disease:e Task Force on the Management
of Valvular Heart Disease of the European Society of Cardiology.
Eur Heart J. 2007;28(2):230– 68.
13. Chandrasekhar S, Tolpin DA, Mangano DT. Chapter30:anesthetic
management of cardiac disease in pregnancy. In Suresh MS, Segal
BS, Preston R, Fernando R, Mason CL, eds. Shnider & Levinson’s
Anesthesia for Obstetrics. 5th ed. Philadelphia :Lippincott Williams
Wilkins; 2013:424– 523.
14. Shime J, Mocarski EJ, Hastings D, Webb GD, McLaughlin PR.
Congenital heart disease in pregnancy:short- and long- term implications. Am J Obstet Gynecol. 1987;156(2):313– 22.
15. Chambers CE, Clark SL. Cardiac surgery during pregnancy. Clin
Obstet Gynecol. 1994;37(2):316– 23.
16. Nussmeier N. Valvular heart disease in the patient undergoing noncardiac surgery. International Anesthesia Research Society Review
Course Lectures. 2010:54– 59. Retrieved from http:// www.iars.
org/ assets/ 1/ 7/ 2010_ IARS_ Review_ Course_ Lectures.pdf.
17. Elkayam U, Bitar F. Valvular heart disease and pregnancy: part
I.Native valves. J Am Coll Cardiol. 2005;46(2):223– 30.
18. Lind J, Wallenburg HC. e Marfan syndrome and pregnancy: a
retrospective study in a Dutch population. Eur J Obstet Gynecol
Reprod Biol. 2001;98(1):28– 35.
19. Sukernik M, Martin DE, Hensley FA, Martin DE, Gravlee
GP. A Practical Approach to Cardiac Anaesthesia. 4th ed.
Philadelphia:Lippincott Williams and Wilkins;2008.
20. Townsley M, Martin ED. Anesthetic management for surgical
treatment of valvular heart disease. In Sukernik MR, Martin DE,
Hensley FA, Martin DE, Gravlee GP, eds. Practical Approach to
Cardiac Anaesthesia. 4th ed. Lippincott Williams and Wilkins;
2008:316– 47.
21. ornhill ML, Camann WR, Harnett M, Mushlin PS, Tsen LC.
Chapter42:Cardiovascular disease. In:Chestnut DH, Wong CA,
Tsen LC, etal., eds., Chestnut’s Obstetric Anesthesia:Principles and
Practice. 5th ed. Saunders; Philadelphia, PA;2014.
22. Silversides CK, Colman JM, Sermer M, Siu SC. Cardiac risk in
pregnant women with rheumatic mitral stenosis. Am J Cardiol.
2003;91(11):1382– 5.
23. de Souza JA, Martinez EE Jr, Ambrose JA, etal. Percutaneous balloon mitral valvuloplasty in comparison with open mitral valve
commissurotomy for mitral stenosis during pregnancy. J Am Coll
Cardiol. 2001;37(3):900– 3.
24. Norrad RS, Salehian O. Management of severe mitral stenosis during pregnancy. Circulation. 2011;124(24):2756– 60.
25. Esteves CA, Munoz JS, Braga S, et al. Immediate and long- term
follow- up of percutaneous balloon mitral valvuloplasty in pregnant patients with rheumatic mitral stenosis. Am J Cardiol.
2006;98(6):812– 6.
26. Gomar C, Errando CL. Neuroaxial anaesthesia in obstetrical patients
with cardiac disease. Curr Opin Anaesthesiol. 2005;18(5):507– 12.
27. Roeder HA, Kuller JA, Barker PC, James AH. Maternal valvular
heart disease in pregnancy. Obstet Gynecol Surv. 2011;66:561– 71.
28. orne SA. Pregnancy in heart disease. Heart. 2004;90:450– 56.
29. Limacher MC, Ware JA, O’Meara ME, etal. Tricuspid regurgitation
during pregnancy: two- dimensional and pulsed Doppler echocardiographic observations. Am J Cardiol. 1985;55:1059– 62.
30. Horlocker TT, Wedel DJ, Rowlingson JC, Enneking FK, American
College of Chest Physicians. Executive summary:regional anesthesia in the patient receiving antithrombotic or thrombolytic therapy:American Society of Regional Anesthesia and Pain Medicine
Evidence- Based Guidelines (ird Edition). Reg Anesth Pain Med.
2010;35(1):102– 5.
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52.
VESSELS
CORONARY ARTERY DISEASE IN PREGNANCY AND
PERIPARTUM ACUTE CORONARY SYNDROME
Eleni Kotsis, Jamie M. Zorn, and GraceLim
CLINICALCASE
A 41- year- old G1P0 female at 36 weeks gestational age
with a past medical history signicant for chronic hypertension, presents to the emergency department with sharp
epigastric pain, 10/ 10 pain that is constant in nature, associated with nausea/ emesis for the last 2 hours. e patient
had limited prenatal care and has not been noncompliant
with antihypertensive therapy for several years. She takes no
home medications.
RISK FACTORS
With a few caveats, the risk factors for an acute coronary process in pregnant women are generally the same
as those typically described in the general population.
Certain inherited autoimmune and connective tissue disorders may exacerbate the risk for ACS in the context of
the physiologic changes of pregnancy. Risk factors include
Kawasaki disease, Marfan syndrome, Loeys– Dietz syndrome, Ehler- Danlos, hypercholesterolemia, obesity,
smoking, diabetes mellitus, increased age, and hypertension. Examining 859 cases in a population- based study
INTRODUCTION
of pregnant women discharged with diagnosis of acute
MI, James et al.3 found in a multivariable regression
Acute coronary syndrome is a constellation of processes that
result from a sudden reduced blood ow to the heart resulting in myocardial ischemia. Major epidemiologic studies
have examined the incidence and timing of acute myocardial infarction (MI) in pregnancy over time. Traditionally,
myocardial ischemia has been considered a rare occurrence in women of childbearing age with an estimated
incidence of 0.6– 1 per 10,000 pregnancies.1 One study
from California that examined pregnancies from 1991 to
2000 placed the incidence at 2.8 per 100,000.2 is rate
appears to be rising, commensurate with the rise in maternal age; a study that looked at births in the United States
over 2000– 2002 found an incidence of 6.2 per 100,000.3
e increasing use of Troponin Ias an indicator of myocardial injury may account for some of the increased incidence
(i.e., increased detection) in the latter study. However, with
recent advances in medicine and social factors leading to
an increase in the average age of women presenting in pregnancy, maternal cardiac issues in the peripartum period are
an increasing concern.
model that diabetes, smoking, and hypertension are sig-
nicant covariates for ACS in pregnancy (adjusted odds
ratios:diabetes 3.6, smoking 8.4, and hypertension 21.7).
Age was found to be independently associated with risk
for ACS in pregnancy, with 30- to 34- year- olds having an
adjusted odds ratio of 6.7 and those older than 35 having
an adjusted odds ratio of 15. rombophilia was another
independent risk factor, with oral contraceptive use oen
identied as the underlying cause, and with blood trans-
fusion and postpartum infection also contributing risk.
Cocaine use, multiparity, hemorrhage, and preeclampsia
have also been noted as risk factors.
3,4
Areview by Roth
etal.5 found that while the ages of pregnant patients with
ACS ranged from 19 to 44years, the majority of patients
(72%) were older than 30. African American women have
a signicantly higher risk for acute MI than other groups
of women. is disparity can be at least partially explained
by the higher incidence of hypertension and preeclampsia
seen in this population, which both separately dramatically increase the risk of acuteMI.
1
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ETIOLOGY
dissections frequently occur in more than one vessel, which
further supports the theory that the blame rests on a sysAcute MI has been reported at all stages of pregnancy, but it
most commonly occurs during the third trimester, in mul-
temic change in physiology, rather than a localized tissue
reaction.
8
tigravid women, and over the anterior wall of the heart. In
a review of reported cases of pregnancy- related acute MI,
atherosclerosis with or without coronary thrombus was
DIAGNOSIS
found in 40% of cases; 21% had a thrombus without evidence of atherosclerosis; 15% had associated dissection;
and 29% of cases had normal anatomy.5 e normal physiologic changes that occur during pregnancy, particularly the
hypercoagulable state and the increased cardiac output, can
exacerbate underlying coronary or myocardial disease.
Postpartum hemorrhage (PPH) can also be a contributing factor for myocardial ischemia. Karpati etal.4 found
that 51% of parturients admitted to their intensive care
unit (ICU) with severe PPH were found to have myocardial ischemia– induced injury, the presence of which correlated strongly with the severity of hemorrhagic shock. e
treatment of early hemorrhagic shock from PPH can avoid
myocardial ischemia. A two- pronged approach involving
(1)increasing myocardial supply (i.e., controlling and treating the hemorrhage), and (2)decreasing myocardial oxygen
demand (the most important determinant of which is heart
rate), is essential.
Preeclampsia and hypertensive disorders of pregnancy
increase the risk of acute MI secondary to enhanced vascular reactivity and endothelial dysfunction that contribute to
coronary atherosclerosis and occlusion. Profound changes
in the coagulation cascade also predispose the parturient
to thrombosis. ese changes include decreased tissue plasminogen activator (t- PA), decreased functional proteins C
and S, and changes in circulating coagulation factor levels.
It has been suggested that patients found to have normal coronary anatomy on angiography aer an ACS event
may have either recovered or had a spontaneously repaired
coronary dissection. One possible explanation for ndings
of coronary occlusion in the absence of atherosclerosis is
coronary vasospasm, resulting in acute coronary thrombosis secondary to the hypercoagulable state of pregnancy.
Coronary dissections are more commonly seen in the postpartum period rather than the antepartum setting, likely
due to natural maternal physiologic changes. ese changes
include an acute increase blood volume and cardiac output,
which increase wall stress on the vessels. e risk of dissection is highest in the third stage of labor and in the acute
postpartum period.
5,7
Excess progesterone may contribute
to spontaneous dissection by causing collagen structural
changes and loss of integrity of the vascular wall. Coronary
Pregnant woman usually present with signs and symptoms
that mirror those of the general population of nonpregnant women who experience an acute MI. ese symptoms
include the acute development of chest pain/ pressure with
radiation to the epigastric area and/ or arm/ shoulder/ neck,
or atypical presentations such as jaw pain. However, the
nonspecicity of shortness of breath and nausea in pregnancy, as well as a presentation of atypical chest pain that
is more common among women in general, make it challenging to diagnose ACS in pregnancy. Women with ACS
may present in a more atypical fashion, specically the lack
of chest discomfort. e dierential diagnosis for these
myriad symptoms is wide, and may include costochondritis,
gastroesophageal reux disease, aortic dissection, and acute
pulmonary embolism. Acute epigastric pain can also be a
symptom of acute fatty liver of pregnancy, preeclampsia, or
HELLP syndrome (hemolysis, elevated liver enzymes, and
low platelets).
Testing to diagnose MI in the pregnant patient is generally the same as in the nonpregnant patient, with a few additional considerations made for gravidity. Electrocardiogram
(EKG) changes and biomarker elevations are similar to
those in nonpregnant patients. Troponin I is still the test
of choice over creatine kinase.9 Adiagnosis is made when
6
there is an elevation in serial cardiac Troponin I, plus any
one of the following:coronary thrombosis on angiography,
new Q- waves, new le bundle branch block, traditional
symptoms, or characteristic ST and/ or T- wave changes.
Coronary angiography during pregnancy is considered safe
at any stage of gestation, and it is the gold standard for diagnosis of coronary artery disease (CAD). During angiography, access by radial artery may be preferred over femoral
access during pregnancy, due to considerations for patient
comfort, ability to position the pregnant patient in le lateral decubitus position more easily, and reduction in bleeding complications.
e symptoms of acute MI are easily mistaken for normal manifestations of pregnancy. erefore, and a high
index of suspicion is essential for early diagnosis. e pregnancy state has been associated with atrial, ventricular,
and supraventricular tachycardia in normal hearts, which
372 SECTION B. CARDIAC CRISES
*Throughout the process, assessment of fetal status and discussion with primary team, patient, and family must occur regarding the risks,
benefits, and goals of treatment. At all tims, appropriate care areas must be notified of the potential urgent need for emergency delivery.
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373
also complicates the diagnosis. Up to 37% of parturients
having elective cesarean sections have been found to have
EKG changes that mimic an acute coronary event, possibly related to the routine use of synthetic oxytocin for the
active management of the third stage of labor.
5
e universal classication of MIs has been revised to
include ve types. Type 1 MI includes spontaneous infarction related to atherosclerotic plaque rupture. Type 2 MI
is secondary to ischemia that leads to myocardial necrosis
and is secondary to such things as endothelial dysfunction,
coronary artery spasm, emboli, and hypo/ hypertension.
Type 3 MI is when death occurs prior to cardiac blood samples being obtained. Type 4a MI is related to percutaneous
coronary intervention (PCI). Type 4b MI is related to stent
thrombosis. Type 5 MI is related to coronary artery bypass
gra (CABG) surgery. e majority of acute MI associated
with pregnancy fall into Type 1 and Type 2MI.
10
As with many obstetric processes, the needs of the mother
and the fetus may be in conict, and therefore the risks,
benets, and alternatives of treatment for both mother and
fetus must be weighed and frankly discussed when considering any treatment modality. In any event, the plan for
managing these situations must be multidisciplinary and
communicative, with input from obstetrics, anesthesiology,
neonatology, emergency medicine, critical care medicine,
and cardiology (see Figure52.1).
Considerations of risk to the fetus must be weighed
against maternal benets with any of the common drugs
used in the management of acute coronary syndromes.
Table 52.1 shows specic drugs and considerations.
In case reports, pregnant patients have safely undergone
early angiography with PCI and/ or coronary stent placement with good outcomes for both the mother and the
11,12
fetus,
e use of bare metal stents (BMS) in pregnant
patients has been described, but there is little data on the
TREATMENT
use of drug eluting stents (DES) in this population currently. Arelative theoretical advantage of BMS over DES is
the decreased time needed with clopidogrel therapy. is is
Treatment of an acute coronary syndrome in pregnancy is
similar to that in the nonpregnant state, with additional
considerations for fetal well- being and delivery planning.
especially important in this patient population, as they are
at risk for scheduled or unscheduled cesarean delivery.
5,13,14
Studies are lacking comparing PCI to thrombolytic therapy
Figure52.1 ACS Algorithm. Throughout
the process, assessment of fetal
status and discussion with primary
team, patient, and family must occur
regarding the risks, benets, and
goals of treatment. At all times,
appropriate care areas must be
notied of the potential urgent need
for emergency delivery. ACS=acute
coronary syndrome; STEMI=ST
elevation myocardial infarction;
NSTEMI=non- ST segment elevation
myocardial infarction; UA=unstable
angina.
Admission
Differential
Diagnosis
EKG
Lab Values
Risk Factors
Diagnosis
Treatment
Follow-Up
Chest Pain
Including ACS
ST Segment
Changes
STEMI
Reperfusion
*Multidisciplinary discussion of delivery planning:
Obstetrics/Cardiology/Anesthesiology/Neonatology
No ST Segment
Changes
Troponin
Positive Negative
High
Risk
NSTEMI UA
Invasive
Low
Risk
Noninvasive
Continuous Evaluation of Fetal Status and Effects on Fetal Well-Being
VESSELS:CORONARY ARTERY DISEASE AND PERIPARTUM ACUTE CORONARY SYNDROME 373
374
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TABLE52.1 COMMONLY USED DRUGS INTHE PREGNANT PATIENT WITHSUSPECTEDACS
Drug Comment
Beta Blockers In pregnancy these are generally considered to be safe. Special considerations for atenolol, based on case reports,
include neonatal hypoglycemia, bradycardia, and respiratory depression, and small for gestational age status with longterm administration.
in this class.
11,12
As with other obstetric management of hypertension, labetalol is thought to be the drug of choice
Fibrinolytics Not been effectively studied in pregnancy at this time. There is an 8% risk for maternal hemorrhage associated with these
Aspirin Low- dose is generally considered safe in pregnancy.
Clopidogrel Safety in pregnancy has not been fully established.
Heparin It is well known that heparin does not cross the placenta and thus cannot directly affect the fetus. Bleeding complications
Nitrates Nitrates are generally well tolerated in pregnancy and can be used for cardiac indications. The usual care to monitor for
ACE Inhibitors These drugs (and angiotensin receptor blockers) are well- known teratogens and should be considered contraindicated in
Statins Cholesterol biosynthesis is considered impor tant in many ways for normal fetal development. HMG- CoA Reductase
Ergot derivatives,
Prostaglandins
in pregnant patients. us, each patient must be considered
on a case- by- base basis to evaluate which method is most
appropriate.
1
Radiation exposure of the fetus is a concern in all pregnancies, but that risk should not delay or prevent the use
of diagnostic/ therapeutic procedures that may be lifesaving for the mother. Techniques to mitigate the amount
of ionizing radiation that the fetus is exposed to should
be employed in these cases. Goldstein and Murphy rst
reported the teratogenic eects of radiation in 1929 while
studying patients that had undergone radiation therapy
for uterine cancer during pregnancy. ey observed a high
rate of microcephaly and reduced cranial circumference.
However, many studies have shown that a 5- rad dose of
fetal radiation at any gestational age is not teratogenic. e
period of highest vulnerability for the fetus is approximately
8– 15 weeks gestational age.15 Coronary angiography has a
radiation exposure to the patient of 2.5– 5.0 mSv, and PCIs
have 5.0– 15.0 mSv exposure. Both of these values are well
below the cuto for teratogenicity at any gestational age.
In addition, the fetus may receive only a percentage of this
radiation, depending on the body parts irradiated and the
type of protection being employed.
Cardiac surgery employing cardiopulmonary bypass
has been performed during pregnancy with varying
13
drugs.
14,15
5,8
in the mother treated with heparin are a concern. Also of concern is the timing of neuraxial techniques for the patient that
is on heparin or low- molecular weight heparin (LMWH).
and treat hypotension must be maintained. Also the tocolytic effects of nitroglycerin must be kept in mind depending on
the patient’s pregnancy course.
this patient population.
inhibitors have not been well studied in this population so current practice is to avoid these drugs until further data
becomes available.
Vasoconstrictive drugs are generally best avoided in this population because of the resultant myocardial strain they can
cause on the mother.
16,17
1
1
1
1
results. Mortality for the mother exceeds that of nonpregnant patients, and the risk of fetal mortality is quite high
with an estimated incidence of 20%– 40%.17 e majority
of data collected about cardiac surgery during pregnancy
has been in patients undergoing valvular surgeries. e
best results have been obtained when surgical intervention occurs during the second trimester. As with most surgical interventions in a pregnant patient, this minimizes
the risk of spontaneous abortion and of teratogenicity
associated with the rst trimester, and the risk of preterm
labor associated with the third trimester. If the fetus is
considered viable, then consideration must be given to
potentially deliver the fetus either before, or during the
cardiac surgery with a double- setup and appropriate fetal
monitoring coordinated.1 Placental perfusion is likely
adversely aected by the nonpulsatile ow of cardiopulmonary bypass (CPB). In one study, increased CPB time
was associated with increased fetal mortality. is was also
related to a longer periods of anoxia. Current recommendations include performing CPB at high ow and at high
pressure, with a normothermic patient, for as little time as
16
possible.
18
If a pregnant patient has moved beyond the acute phase
of an MI, then sometimes it may be in her best interest to
delay delivery for two or three weeks to allow for some
374 SECTION B. CARDIAC CRISES
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375
degree of myocardial recovery. Clinical trials evaluating
the optimal timing for delivery or surgical interventions in
the setting of an acute or recent MI are lacking. Maneuvers
that will decrease cardiac workload at the time of labor
and delivery are advisable. ese include early epidural
anesthesia with gradual dosing to avoid hypotension, le
uterine displacement to avoid aortocaval compression, and
supplemental oxygen if necessary. In addition, avoidance
and management of extremes of blood pressure and heart
rate, and possibly an assisted second stage of labor to avoid
the hemodynamic eects of prolonged Valsalva maneuvers
are recommended. Regardless of the timing and mode of
delivery, it is essential that this be a multidisciplinary eort
involving cardiology, cardiothoracic surgery, maternal fetal
medicine obstetrics, neonatology, obstetric anesthesiology,
and critical care medicine.
1,5,19
death of the mother and delivery. Delivery times greater
than 15 minutes aer maternal death resulted in fetal death
in all cases. In contrast, all surviving infants delivered within
5 minutes aer maternal death were healthy. To maximize
the chances of survival for both the mother and infant, perimortem cesarean delivery within 5 minutes of cardiac arrest
is recommended.
21
e timing of discharge aer an acute MI in the antepartum period needs to be determined on an individual
basis. Athird- trimester parturient may require continued
hospitalization and a modestly restricted level of activities secondary to the increased myocardial consumption.
She may also require evaluation of fetal distress during
physical activity and more frequent assessment of fetal
maturity.
5,7
For the parturient who has had an antepartum MI,
delivery should be postponed, if possible, for 2– 3 weeks
COMPLICATIONS
aer the event to allow for adequate myocardial recovery. e increased hemodynamic lability and uterine contractions cause signicant volume shis and myocardial
Complications beyond the immediate initial cardiac event
can range from minimal to long- term serious concerns.
Adverse events can be divided into those that are ischemic
(i.e., unstable angina, MI, ventricular arrhythmias, or cardiac arrest) and nonischemic in origin. Ischemic cardiomyopathy can result with subsequent congestive heart failure
with long- term sequelae. Cardiac arrest, especially around
the time of delivery, is also a major concern, and ACLS protocols for the pregnant patient should be followed in this
event. Atrial arrhythmias requiring treatment are another
possible outcome. Subsequent stroke and pulmonary
embolus have also been described. In addition to maternal
complications, there are fetal and neonatal eects associated with cardiac events during pregnancy. ese include
premature birth, low birth weight/ intrauterine growth
restriction, neonatal respiratory distress, spontaneous abortion, intraventricular hemorrhage, and death.
20
demands during labor and delivery, which can increase the
risk for myocardial ischemia and cardiac decompensation.
In addition, the reduced oncotic pressure and increased
capillary interstitial pressure associated with pregnancy,
coupled with inadequate myocardial contractility aer
acute MI, may lead to pulmonary edema. e appropriate mode of delivery in the parturient with gestational
MI should be determined on a case- by- case basis. Review
of outcomes of 150 cases found no convincing evidence
to support one method of delivery versus the other.8 Both
vaginal and cesarean deliveries have advantages and disadvantages. Advantages of elective cesarean section include
enhanced control over the timing of delivery and avoidance
of potentially prolonged dysfunctional labor and its associated hemodynamic consequences. Vaginal delivery eliminates the risks associated with abdominal delivery including
major shis in uids, blood loss, thrombosis, infection, and
postoperative recovery. An assisted vaginal delivery at the
PROGNOSIS AND DELIVERY PLANNING
e maternal mortality rate presented by Hankins and colleagues found an overall mortality rate of 37% from myocardial infarction in pregnancy, and fetal loss was reported
in 34%.15 Roth etal. found a fetal mortality of 9% (6 out of
68), with the majority of fetal deaths being associated with
maternal mortality. In the context of maternal cardiac arrest
leading to perimortem cesarean delivery, survival of the
infant is directly proportional to the time interval between
second stage of labor is recommended to reduce cardiac
load and oxygen demands in a subset of parturients who
suered antepartumMI.
5,7
ere is limited data on maternal and fetal outcomes in
patients with remote history of MI. Reported cases of pregnancy and prior MI are limited, but it appears that a prior
history of MI is not associated with increased risk of maternal death. e risks associated with subsequent pregnancies
depend on many factors including the amount of myocardial necrosis, residual le ventricular function, underlying
anatomy, and ongoing myocardial ischemia.
5
VESSELS:CORONARY ARTERY DISEASE AND PERIPARTUM ACUTE CORONARY SYNDROME 375
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