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Trang 8Critical Care Obstetrics, 5th edition Edited by M Belfort, G Saade,
M Foley, J Phelan and G Dildy © 2010 Blackwell Publishing Ltd
Michael R Foley 1 , Roxann Rokey 2 & Michael A Belfort 3
1 Scotsdale Healthcare, Scottsdale, Arizona and Department of Obstetrics and Gynecology, University of Arizona College of
Medicine, Tucson, AZ, USA
2 Department of Cardiology, Marshfi eld Clinic, Marshfi eld, WI, USA
3 Department of Obstetrics and Gynecology, Division of Maternal - Fetal Medicine, University of Utah School of Medicine,
Salt Lake City, UT and HCA Healthcare, Nashville, TN, USA
Introduction
Although cardiac disease complicates only 1 – 4% of all
pregnan-cies in the United States, such conditions continue to account for
up to 10 – 25% of maternal mortality [1 – 5] Similar fi ndings are
seen elsewhere In the recently published Confi dential Enquiry
into maternal deaths, Why Mothers Die , 2000 – 2002, heart disease
has now become the leading cause of indirect maternal death in
the UK In contrast to the very distant past, rheumatic fever and
its valvular sequelae of heart failure is no longer the most common
cause of maternal mortality Both maternal congenital heart
disease and acquired maternal heart disease such as myocardial
infarction and cardiomyopathy now are the predominant causes
of maternal death With advances in the treatment of congenital
heart disease in newborns and children, more young women are
reaching reproductive age and attempting pregnancy As a
con-sequence, congenital heart disease is a common form of heart
disease complicating pregnancy in North American women On
the other end of the spectrum, more women are postponing
pregnancy until the fourth or fi fth decade of life – a time where
underlying medical conditions such as hypertension and
diabe-tes, coupled with advancing maternal age, may exacerbate the
incidence of acquired heart disease (such as myocardial infarction
or cadiomyopathy) complicating pregnancy Indeed, in the UK,
maternal mortality rates from congenital causes have remained
stable but those from ischemia/cardiomyopathy have risen
The long held belief that pregnancy is absolutely
contraindi-cated in maternal cardiovascular diasease is no longer justifi able
using evidenced - based medicine There are some conditions in
which pregnancy is contraindicated and a high maternal risk and
poor fetal outcome can be predicted However, in many women
with heart disease a more favorable maternal and fetal outcome
will be expected.This chapter, therefore, will focus on the
precari-ous interaction between cardiac disease and pregnancy
Counseling the p regnant c ardiac p atient
Maternal outcome in the cardiac patient is dependent upon the type of cardiac disease, myocardial function, maternal functional status, presence and severity of cyanosis, pulmonary vascular pressures/resistance and prior surgical procedures along with any uncorrected lesions and residuae or sequelae of repair Of these, maternal functional status, the degree of cyanosis along with accompanying pulmonary vascular pressure/resistance, and the type of current maternal cardiac disease are the most predictive
of an adverse outcome Siu et al [6] have reported a method of assessing risk and outcomes in women with cardiac disease using (i) functional status, (ii) left heart dysfunction, (iii) prior cardiac events, and (iv) left heart obstruction as indicators of who is at a level of risk that can safely allow delivery at a community hospital
Before 1973, the Criteria Committee of the New York Heart Association (NYHA) recommended a classifi cation of cardiac disease based on clinical function (classes I – IV) Table 20.1 out-lines the specifi cs of the NYHA classifi cation system Such a clas-sifi cation is useful in discussing the pregnant cardiac patient, although patients who begin pregnancy as functional class I may develop congestive heart failure and pulmonary edema during the course of gestation Other classifi cations including the Canadian Cardiovascular Society Functional Classifi cation (classes I – IV) and Specifi c Activity Scale have been used in other countries and have similar grades of disability
This functional classifi cation system, although somewhat anti-quated, remains most useful when comparing the performance
of individuals with uniform etiologic and anatomic defects In general, most women who begin pregnancy as a functional class NYHA I or II have an improved outcome as compared with those classifi ed as class III or IV [7]
Counseling the pregnant cardiac patient regarding her prog-nosis for successful pregnancy is further complicated by recent advances in medical and surgical therapy, fetal surveillance, and neonatal care Such advances render invalid many older estimates
of maternal mortality and fetal wastage Table 20.2 represents a
Trang 9Currently available data suggest that today maternal mortality
is almost exclusively seen in patients with pulmonary hyperten-sion, cardiac valvular disease (acquired or congenital) and includ-ing endocarditis, coronary artery disease, cardiomyopathy, and sudden cardiac arrhythmia death DeSwiet, reporting on mater-nal mortality from heart disease in the United Kingdom between
1985 and 1987, stated that all deaths occurred due to endocarditis (22%), pulmonary hypertension (30%), coronary artery disease (39%), and cardiomyopathy or myocarditis (9%) [2] Similarly,
a review of maternal mortality in Utah from 1982 to 1994 revealed
13 cardiac deaths, 4 (31%) due to pulmonary hypertension, 4 secondary to cardiomyopathy (31%), 2 due to coronary artery disease (15%), and 3 (23%) due to sudden arrhythmia [9] In a smaller series of maternal deaths from West Virginia between
1985 and 1989, the two cardiac deaths described were due to cardiomyopathy [10] Clark et al [11] reported on 95 maternal deaths within a large USA community hospital system in which 1.46 million deliveries occurred over a 6 - year period (2000 – 2006) Cardiac disease accounted for 11% of all deaths (n = 10) and was the fourth most common cause of death after complications of pre - eclampsia, amniotic fl uid embolism, and obstetric hemor-rhage) Of interest is that 50% of the cardiac deaths were associ-ated with myocardial infarction in women with no prior history
of ischemic heart disease
In a study of 252 pregnancies in women with cardiac disease the following independent predictors of cardiac events (conges-tive heart failure, arrhythmia, and stroke) were identifi ed [12] :
• NYHA functional class III or IV
• maternal cyanosis
• history of prior arrhythmia
• pulmonary vascular disease
• myocardial dysfunction (ejection fraction < 40%)
• left heart obstruction
The same authors then prospectively applied these risk predic-tors to another cohort of women with congenital or acquired cardiac disease and found that the four predictors of having cardiac events were:
• left ventricular systolic dysfunction (LVEF < 40%)
• poor functional status/cyanosis
• previous cardiac event (heart failure, stroke, transient ischemic attack)
• left - sided cardiac valvular lesions (mitral valve area < 2.0 cm 2 , aortic valve area < 1.5 cm 2 )
One point was given for each fi nding Not suprisingly, those with scores of 0 and no specifi c risk issue had the lowest risk of developing pulmonary edema, stroke, arrhythmia necessitating treatment, cardiac arrest or death
In a study by Presbitero et al [13] , looking at the outcome of the mother and the fetus in pregnancies complicated by cyanotic congenital heart disease, the adverse impact of low maternal oxygen saturation was clearly illustrated The likelihood of a live birth was less frequent (12%) if the mother ’ s resting oxygen satu-ration was below 85% as compared to a resting oxygen satusatu-ration
of greater than 85% (63%) It would appear, however, that with
synthesis of maternal risk estimates for various types of cardiac
disease that was initially developed for the fi rst edition of this text
in 1987 Counseling of the pregnant cardiac patient, as well as
general management approaches, were based on this classifi
ca-tion [8] Category I included condica-tions that, with proper
man-agement, were associated with negligible maternal mortality
(1%) Cardiac lesions in category II traditionally carried a 5 – 15%
risk of maternal mortality Patients with cardiac lesions in group
III were, and probably remain, subject to a mortality risk
exceed-ing 25% In all but exceptional cases, this risk is unacceptable,
and prevention or interruption of pregnancy is generally
recommended
Table 20.1 New York Heart Association ( NYHA ) functional classifi cation
system
Class I No limitations of physical activity, ordinary physical activity does
not precipitate cardiovascular symptoms such as dyspnea,
angina, fatigue, or palpitations
Class II Slight limitation of physical activity Ordinary physical activity will
precipitate cardiovascular symptoms Patients are comfortable
at rest
Class III Less than ordinary physical activity precipitates symptoms that
markedly limit activity Patients are comfortable at rest
Class IV Patients have discomfort with any physical activity Symptoms are
present at rest
Table 20.2 Maternal risk associated with pregnancy
Group I: Minimal risk of complications (mortality < 1%)
Atrial septal defect *
Ventricular septal defect *
Patent ductus arteriosus *
Pulmonic/tricuspid disease
Corrected tetralogy of Fallot
Bioprosthetic valve
Mitral stenosis, New York Heart Association (NYHA) classes I and II
Marfan syndrome with normal aorta
Group II: Moderate risk of complications (mortality 5 – 15%)
Mitral stenosis with atrial fi brillation †
Artifi cial valve * †
Mitral stenosis, NYHA classes III and IV
Aortic stenosis
Coarctation of aorta, uncomplicated
Uncorrected tetralogy of Fallot
Previous myocardial infarction
Group III: Major risk of complications or death (mortality > 25%)
Pulmonary hypertension
Coarctation of aorta, complicated
Marfan syndrome with aortic involvement
* If unassociated with pulmonary hypertension
† If anticoagulation with heparin, rather than coumadin, is elected
Trang 10tion) at a time when optimum anticoagulation with coumarin derivatives may have adverse fetal consequences Table 20.4 out-lines the relative changes in the coagulation factors and inhibitors associated with normal pregnancy For women receiving any type
of therapeutic anticoagulation, the risk of serious postpartum hemorrhage is also increased
4 Marked fl uctuations in cardiac output normally occur in
preg-nancy, particularly during labor and delivery [16] Such changes increase progressively from the fi rst stage of labor, reaching, in
appropriate obstetric care, the presence or absence of the
afore-mentioned secondary complications of cardiomyopathy,
pulmo-nary hypertension, endocarditis, and sudden arrhythmias play a
much more important role in determining ultimate maternal
outcome than the primary structural nature of the cardiac lesion
itself
Physiologic c onsiderations
The unique problems encountered by the pregnant woman with
cardiac disease are secondary to four principal physiologic
changes [14]
1 A 50% increase in intravascular volume is seen in normal
preg-nancy Figure 20.1 illustrates the changes in total blood volume,
plasma volume, and red cell volume during normal pregnancy
In patients whose cardiac output is limited by intrinsic
myocar-dial dysfunction, valvular lesions, or ischemic cardiac disease,
volume overload will be poorly tolerated and may lead to
conges-tive failure or worsening ischemia In patients with an anatomic
predisposition, such volume expansion may result in aneurysm
formation or dissection (e.g Marfan syndrome) Even in women
with multiple pregnancies, the heart is able to withstand
repeti-tive episodes of gestational volume overload without lasting
det-rimental structural or functional changes [15]
2 Decreased systemic vascular resistance (SVR) becomes especially
important in patients with the potential for right to left shunts,
which will invariably be increased by a falling SVR during
preg-nancy Such alterations in cardiac afterload also complicate
adap-tion to pregnancy in patients with certain types of valvular
disease Table 20.3 summarizes the central hemodynamic changes
associated with normal term pregnancy
3 The hypercoagulability associated with pregnancy heightens the
need for adequate anticoagulation in patients at risk for arterial
thrombosis (artifi cial valves and some subsets of atrial fi
brilla-5,000
4,000
3,000
2,000
Weeks of pregnancy
Total blood volume
Plasma volume
Red blood cell volume
Figure 20.1 Changes in total blood volume, plasma volume, and red cell
volume in normal pregnancy (Reproduced by permission from Shnider SM, Levinson G Anesthesia for Obstetrics , 3rd edn Lippincott, Williams & Wilkins, 1993.)
Non - pregnant Pregnant Percent change *
Cardiac output (L/min) 4.3 ± 0.9 6.2 ± 1.0 +43
Heart rate (bpm) 71 ± 10.0 83 ± 1.0 +17
Systemic vascular resistance (dyne/cm/sec 5 ) 1,530 ± 520 1,210 ± 266 − 21
Pulmonary vascular resistance (dyne/cm/sec 5
) 119 ± 47.0 78 ± 22 − 34 Colloid oncotic pressure (mmHg) 20.8 ± 1.0 18.0 ± 1.5 − 14
COP − PCWP (mmHg) 14.5 ± 2.5 10.5 ± 2.7 − 28
Mean arterial pressure (mmHg) 86.4 ± 7.5 90.3 ± 5.8 − NSC
Pulmonary capillary wedge pressure (mmHg) 6.3 ± 2.1 7.5 ± 1.8 − NSC
Central venous pressure (mmHg) 3.7 ± 2.6 3.6 ± 2.5 NSC
Left ventricular stroke work index (g/m/m 2
) 41 ± 8 48 ± 6 +NSC
* NSC = no statistically signifi cant change
COP − PCWP = colloid oncotic pressure − pulmonary capillary wedge pressure (mmHg)
(Reproduced by permission from Clark SL, et al: Central hemodynamic assessment of normal term pregnancy Am
J Obstet Gynecol 1989;161:1439.)
Table 20.3 Central hemodynamic changes
associated with normal term pregnancy