Download Simulating cardiac disease

Cardiac Diseases in
Pregnancy
1
The incidence and changing
pattern of heart disease
• It ranges from 0.1% to 4%.
• Hospital statistics - industrialized
countries have shown a decrease in
the incidence from 0.9% to 0.3%
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Incidence of heart disease………
Sharp decline in the incidence of chronic
rheumatic heart disorders.
Advances in the medical and surgical
treatment of patients with congenital heart
defects has resulted in an increased
survival to reproductive age.
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Maternal mortality from heart
disease
• Statistics have demonstrated a decline in
maternal mortality from cardiac disease
since 1950 from 5.6 to 0.3 per 100 000
births.
• B’s of improved medical care of the
pregnant cardiac patient and a sharp
decrease in the incidence of rheumatic
heart disease.
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Maternal mortality from heart disease
• Confidential enquiry of latest report on maternal
deaths in the United Kingdom, has shown that
cardiac disease accounted for the greatest
number of maternal deaths
• accounting for 35 (16.5%) of all maternal deaths
over the period 1997–99*
• (37 of 323) in the 1991 to 1993 triennium
• (18) -1988 to 1990 trienniums
• (23) -1985 to 1987
* de Swiet M. Cardiac disease. In: Lewis G, Drife J, eds. Why Mothers Die 1997–1999. The Confidential Enquiries into Maternal Deaths in the United
Kingdom. London: Royal College of Obstetricians and Gynaecologists, 2001; 153–64
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Maternal mortality from heart disease
Cardiac diseases is also the leading
cause of indirect maternal death. Of
the cardiac deaths reported to the
Confidential enquiry between 20002002, 40% were noted to have
substandard care.
Deans CL, Uebing A, Steer PJ. Cardiac disease in pregnancy. In Progress in
Obstetrics and Gynaecology, Vol 17, Edi Studd J, Tan S L, Chervenak FA.Churchill
Livingstone 2007, 164-182.
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Cardiovascular Physiology of
Pregnancy
• Normal pregnancy is associated with an
increase of 30 to 50 percent in blood volume
• Blood volume increases, starting at the sixth
week and rising rapidly until mid pregnancy; the
levels peak by 20 to 24 weeks of pregnancy and
then are either sustained until term or decrease
An estrogen-mediated stimulation of the reninangiotensin system results in sodium and water retention
appears to be the mechanism underlying the blood
volume increase.
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Cardiovascular Physiology of
Pregnancy
• Increase in cardiac output is most significant
change during pregnancy.
• It begins to rise in first trimester and steadily
rises to peak at 32 weeks by 30 to 50%.
• Cardiac output is normally 4.2 L/min., is 6.5
L/min. at 8-10 weeks of pregnancy and remains
so till near term.
• Increase in cardiac output is achieved by rise in
stroke volume (in early pregnancy) and Heart
Rate (in latter part of pregnancy) adjusting
together
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Cardiovascular Physiology of Pregnancy
• Due to rise in endogenous circulating
catecholamine, there is positive inotropic and
chronotropic myocardial response.
• Later in pregnancy, the rise is related to an
acceleration of heart rate (25%), since stroke
volume decreases as a result of vena caval
compression.
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• Blood Pressure remains almost to
prepregnant levels except a tendency to
fall during pregnancy (particularly during
midtrimester) as the systemic
vascular/peripheral resistance falls
(due to large arteriovenous shunts at
placental bed and physiologic vasodilation
secondary to endothelial prostacyclin and
circulating progesterone)
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• Colloid oncotic pressure is another
important variable
• Both plasma and interstitial colloid oncotic
pressure decrease throughout pregnancy
• There is accompanying increase in
capillary hydrostatic pressure.
• An increase in hydrostatic pressure or a
decrease in colloid oncotic pressure may
overcome the delicate balance that favors
oedema formation
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Colloid oncotic pressure
• After delivery, decrease in plasma colloid
oncotic pressure takes place reaching a
peak between 6 to 16 hours and returns
towards intrapartum level after 24 hours.
• These changes can lead to dependant
oedema complicating diagnosis of cardiac
decompensation.
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Simulating cardiac disease
Owing to these normal changes, many
healthy pregnant women have symptoms
mimicking those of cardiac disease,
Including:
fatigue, dyspnea, and light-headedness,
& number of “abnormal” findings on physical
examination, electrocardiography, and
echocardiography
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Table 1. Normal physiological changes of pregnancy
that mimic symptoms and signs of cardiac disease
Symptoms
Tiredness
Dyspnoea
Orthopnoea
Syncope
Light-headedness
Physical signs
Peripheral oedema
Hyperventilation
Distended neck veins with prominent A and V
waves
Brisk, diffuse, and displaced left ventricular
impulse
Palpable right ventricular impulse
Increased S1 intensity
Persistent splitting of S2
Early ejection systolic murmurs at lower left
sternal edge or pulmonary area
Cervical venous
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Mammary souffle
Contd..
Table 1. Normal physiological changes of pregnancy
that mimic symptoms and signs of cardiac disease
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Electrocardiogram
Left axis deviation
ST segment and T wave changes
Small Q, inverted P or T wave in lead III
Increased R wave amplitude in lead V2
Atrial or ventricular ectopics
Chest X-ray
Straightened left upper cardiac border
Horizontal heart position
Increased lung markings
Echocardiogram
Increased left/right ventricular dimensions
Mild increase in left/right atrial size
Slightly improved left ventricular systolic function
Functional tricuspid/pulmonary insufficiency
Small pericardial
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Management areas
Areas be considered in the clinical approach to
the woman with heart disease who is pregnant
or considering pregnancy:
1) Risk stratification, Pre-conceptional
2) Antepartum management,
3) Peripartum management,
4) Recurrence of congenital lesion in the neonate,
5) Site of antepartum and peripartum care.
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Pre-conceptional counselling
• This is an important aspect of
management or the cardiac patient
planning a pregnancy.
• Ideally, the obstetrician and cardiologist
should work together to help the patient
make an informed decision.
• Prevent an unwanted pregnancy and
avoid the risks associated with pregnancy
continuation or termination.
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Risk assessment
• Poor functional status (NYHA class III or
IV) or cyanosis
• Left ventricular systolic dysfunction (ejection
fraction < 0.40)
• Left heart obstruction (mitral valve area
<2.0 cm2, aortic valve area < 1.5 cm2, or
peak left ventricular outflow tract gradient
> 30 mm Hg)
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Risk assessment
A cardiac event (arrhythmia, stroke,
transient ischemic attack, or
pulmonary edema) before pregnancy
but since a prior cardiac surgical
procedure.
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Risk assessment
Siu developed a risk index incorporating
these factors.
In a woman with heart disease and no other risk
factors, the likelihood of a cardiac event during
pregnancy is about 5%, increasing to 25% with one
risk factor & 75% with more than one risk factor.
Siu SC, Sermer M, Colman JM, et al. Prospective multicenter
study of pregnancy outcomes in women with heart disease.
Circulation 2001; 104:515–521.
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Table 2. Maternal mortality risk and cardiac disease
Group
Cardiac disease
Associated mortality risk
I
Atrial septal defect*
<1%
Ventricular septal defect*
Patent ductus arteriosus*
Pulmonary/tricuspid valve disease
Corrected tetralogy of Fallot
Bioprosthetic valve
Mitral stenosis, NYHA Class I, II
II
Coarctation of aorta without valvular involvement 5% - 15%
Uncorrected tetralogy of Fallot
Marfan’s syndrome with normal aorta
Mechanical prosthetic valve
Mitral stenosis with atrial fibrillation or NYHA Class III, IV
Aortic stenosis
Previous myocardial infarction
III
Pulmonary hypertension—primary or secondary 25% - 50%
Coarctation of aorta with valvular involvement
Marfan’s syndrome with aortic involvement
Peripartum cardiomyopathy
*Uncomplicated
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• A careful history is obtained to identify
previous cardiac complications.
• The patients functional status as per The
New York Heart Association(NYHA) is
defined
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Table 3.NEW YORK HEART ASSOCIATION FUNCTIONAL
CLASSIFICATION OF CARDIAC DISEASE
CLASS I
No functional limitation of activity.
No symptoms of cardiac decompensation with activity.
CLASS II
Mild amount of functional limitation.
Patients are asymptomatic at rest. Ordinary physical activity
results in symptoms.
CLASS III
Limitation of most physical activity.
Asymptomatic at rest
Minimal physical activity results in symptoms.
CLASS IV
Severe limitation of physical activity results in symptoms.
Patients may be symptomatic at rest/heart failure
at any point of pregnancy.
CLASS V
If patient is on ionotropic support, ventilator, Assisted
circulation or having comprised renal or pulmonary
function necessitating dialysis/EMCO to
maintain vital signs.
The criteria committee of the New York Heart Association, Nomenclature and criteria for diagnosis of diseases of heart and great vessels,
Edi 8, New York Association,1979.
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Antepartum Care
• The chief aim of management of the
patient in pregnancy is to keep patient
within her cardiac reserve.
• It is preferable to have detailed baseline
information prior of pregnancy.
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Antepartum care
• Limiting activity is helpful in severely
affected women with ventricular
dysfunction,
• left heart obstruction, or class III or IV
symptoms.
• Hospital admission by mid-second
trimester may be advisable for some.
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Antepartum care
• Problems should be identified early
and treated aggressively, especially
pregnancy induced hypertension,
hyperthyroidism, infection, and anemia.
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Table 4. Recommended antibiotic prophylaxis for high-risk women undergoing
genitourinary or gastrointestinal procedures
Category
Drug and dosage
High-risk patient
Ampicillin, 2 g IM or IV,
plus
gentamicin sulfate (Garamycin), 1.5 mg/kg IV 30 min before
procedure; ampicillin, 1 g IV, or amoxicillin (Amoxil,
Trimox, Wymox), 1 g PO 6 hr after procedure
High-risk patient
who has
penicillin allergy
Vancomycin HCl (Vancocin, Vancoled), 1 g IV over 2 hr,
plus
gentamicin sulfate, 1.5 mg/kg IV 30 min before procedure
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Antepartum care
Beta-blockers rather than digoxin should be used to
control the heart rate for patients with functionally
significant mitral stenosis.
Empiric therapy with beta-blockers is offered
to patients with coarctation, Marfan syndrome,
and ascending aortopathy for other reasons (eg, a
bicuspid aortic valve).
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Arrhythmias should be treated if warranted
Premature atrial or ventricular beats are common
in normal pregnancy, and in patients with
preexisting arrhythmias,
Pregnancy may exacerbate their frequency and
hemodynamic severity.
These usually are not treated.
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Antepartum care
Sustained tachyarrhythmias, such as
atrial flutter or atrial fibrillation, should be
treated promptly.
If possible, all antiarrhythmic drugs should
be avoided during the first trimester, and those
known to be teratogenic should be avoided
throughout pregnancy.
Because of their safety profiles, preferred drugs
include digoxin, beta-blockers and adenosine.
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Antepartum care
• Anticoagulation therapy. No current
strategy is equally safe for both mother
and fetus.
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Anticoagulation therapy
Oral therapy with warfarin is effective and
logistically easy.
However, it can affect embryonic organ
development, although some evidence shows
that a dosage of 5 mg per day may not be
teratogenic.
Fetal intracranial bleeding is a risk throughout
pregnancy, particularly during vaginal delivery,
unless warfarin is stopped before labor.
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Anticoagulation therapy
* Heparin in adjusted subcutaneous doses
does not cross the placenta and so has no
teratogenic effects.
However, it may cause maternal
thrombocytopenia and osteoporosis and is
less effective in preventing thrombosis in
patients with prosthetic valves.
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Anticoagulation therapy
More recent guidelines recommend either
(1) adjusted-dose heparin during the entire pregnancy or
(2) adjusted-dose heparin until the 13th week of gestation,
warfarin from the 14th week to the middle of the third
trimester, and then restart adjusted-dose heparin.
* Low-molecular-weight heparin in adjusted
doses is easier to administer and has been
suggested as an alternative to adjusted-dose
unfractionated heparin.
Bates SM, Greer IA, Hirsh J, Ginsberg JS. Use of antithrombotic agents during pregnancy. Chest 2004; 126:627S–
.
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Anticoagulation therapy
At week 36 #
*Discontinue warfarin
*Change to UFH titrated to a therapeutic aPTT or antifactor Xa level.
At Delivery:
*Restart heparin therapy 4 to 6 hr after delivery if no
contraindications
*Resume warfarin therapy the night after delivery if no
bleeding complications
#if labor begins while the woman is receiving warfarin,
anticoagulation should be reversed and caesarean
delivery performed
Ginsberg JS, Greer I, Hirsh J. Use of antithrombotic agents during pregnancy. Chest 2001;119:Suppl:122S-131S
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Anticoagulation therapy
Monitoring
• With LMWH administered sc. twice daily
maintain anti-Xa level between 0.7 and
1.2 U/ml 4 hours after admn.
• With dose adjusted UFH, the aPTT should be at
least twice control.
• those on warfarin, the INR goal should be
3.0(range 2.5 to 3.5)
Chan WS, Anand S, Ginsberg JS. Anticoagulation of pregnant women with mechanical heart valves: a systematic
review of the literature. Arch Intern Med 2000;160:191-196
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Peripartum management
• Cesarean section is indicated only for the
following conditions:
• Aortic dissection
• Marfan syndrome with dilated aortic root
• Taking warfarin within 2 weeks of labor.
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Peripartum care
Preterm induction is uncommon.
However, once fetal lung maturity is
assured,
a planned induction and delivery may be
warranted for high-risk patients to ensure
that appropriate staff and equipment are
available.
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Peripartum care
Antibiotic prophylaxis for endocarditis is
not routine. AHA guidelines do not recommend routine
endocarditis prophylaxis for cesarean section delivery or
for uncomplicated vaginal delivery without infection.37
However, some centers do administer
endocarditis prophylaxis for vaginal delivery
in women with structural heart disease, as an
uncomplicated delivery cannot always be
anticipated.
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Peripartum care
Positioning the patient on her left
side
lessens the hemodynamic fluctuations
associated with contractions when the
patient is supine.
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Peripartum care
• Forceps or vacuum extraction should be
considered at the end of the second stage
of labor to shorten and ease delivery.
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Peripartum care
• Postpartum monitoring
Because hemodynamics do not return to
baseline for many days after delivery,
patients at intermediate or high risk may
require monitoring for at least 72 hours
postpartum.
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Peripartum care
• Lactation should be encouraged unless
patient is in failure.
• Cardiac output is not compromised during
lactation.
• Lactation is a pathway for fluid excretion
and diuretic requirement may actually fall.
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Contraception
• Barrier methods – unreliable.
• COC contraindicated.
• Progesterone only pill have better side effect
profile & long acting slow releasing as Mirena
intrauterine system have improved efficacy.
• Sterilization where family completed.
(Laparoscopic clip sterilization carries risk).
Deans CL, Uebing A, Steer PJ. Cardiac disease in pregnancy. In Progress
in Obstetrics and Gynaecology, Vol 17, Edi Studd J, Tan S L,
Chervenak FA.Churchill Livingstone 2007, 164-182.
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Conclusion
Pregnancy causes significant haemodynamic
changes and imposes an additional burden on
the cardiac patient, especially around the time of
labour and in the immediate puerperium.
To achieve a successful pregnancy outcome, a
clear understanding of these haemodynamic
adaptations as well as meticulous maternal and
foetal surveillance for risk factors and
complications throughout the pregnancy is
essential.
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Conclusion
Appropriate contraceptive and family planning
advice as well as pre-conceptional counselling
are also important.
The concerted efforts of a team consisting of the
obstetrician, cardiologist, anaesthetist,
cardiothoracic surgeon, neonatologist, and
paediatric cardiologist are mandatory to ensure
optimal results.
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