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CARDIOVASCULAR DISEASES IN PREGNANCY

Increase in the intensity of first heart sound with


exaggerated splitting

May have systolic ejection flow murmurs

Diastolic murmurs are rare and would warrant further


study

Joanna Zerline Lozada-Pascual, MD, FPOGS, FPSMFM


Department of OB-GYN
12 July 2011

Heart Disease

Increase in blood volume by 40 to 60% starting early in first


trimester, mainly due to expansion of plasma volume
Cardiac output increases by 40 to 50% beginning in first trimester,
with peak at the 20-24th week, initially due to SV increase, later
due to HR increase
Peripheral vascular resistance decreases during pregnancy
causing a decrease in diastolic blood pressure, especially in the
early trimester

Increase in heart size due to eccentric hypertrophy

BP declines in mid-pregnancy due to decreased total peripheral


resistance and the rise in cardiac output.

*Patients who fail to exhibit a drop in BP are more


likely to develop preeclampsia.

During labor : 500 ml of blood is autotransfused into maternal


circulation resulting in increased BP and cardiac output.

Peaks of Cardiac Activity during Pregnancy

These are during the early third trimester, during labor, during
delivery and during the puerperium.

Changes in Diagnostic Tests Findings during Pregnancy

1.

Chest X-ray Film

Lordosis can create straightening of the left upper


cardiac border, mimicking left atrial
enlargement

Elevation of the diaphragm causes more horizontal


position of the heart

Pulmonary vasculature appears more prominent

Leading cause of death in women who are 25-44 yrs old

Cardiovascular physiology

2.

normal pregnancy,
functional systolic heart murmurs are common; respiratory effort
is accentuated and at times suggests dyspnea; edema in the lower
extremities after midpregnancy is common; and fatigue and
exercise intolerance develop in most women

3. Electro-cardiogram

Horizontal position of the heart causes left or right


shift of QRS

Transient ST-segment an t-wave changes are common

Right axis deviation, RBBB, or ST depression of 1 mm


on left precordial leads

Q waves in lead III, T wave inversion in III, V2 and V3

Small decreases of PR and QT

Rotation of =/- of 15 degrees (QRS axis)

Atrial and ventricular premature contractions are


relatively frequent

Pregnancy does not alter voltage findings

4. Echocardiogram

allows noninvasive evaluation of structural and


functional cardiac factors

Increase in end-diastolic and end-systolic ventricular


measurements with no increase in wall thickness

Mild tricuspid regurgitation may be due to increase


volume

Increased Trivial tricuspid regurgitation (43 to 94% at


term)

Pulmonary regurgitation (94% at term)

Increased left atrial size by 12 to 14%

Increased LV end diastolic dimensions by 6-10%

Inconsistent increase in LV thickness / left ventricular


mass

Pericardial effusions

5. Pulmonary artery catheterization no change

Cardiac Physical Examination


Clinical Findings of HD

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SYMPTOMS

cardiologist. These patients


may have to be admitted, as
one-third of them will
decompensate to class IV.
Labor must be in the
hospital. Counseling on the
risk of pregnancy must be
made.
Severely compromised.
Unable to perform any
physical activity without
discomfort. Symptoms are
present at rest and are
increased with any physical
activity.
Treat the decompensation,
and then manage any
obstetric problem. This is
associated with high
maternal mortality rate.
Close coordination with the
cardiologist is made.
Counseling on the risk of
pregnancy is made.

Severe or progressive dyspnea


Nocturnal cough
Hemoptysis
Syncope with exertion

Class
IV

Chest pain related to effort or exertion

CLINICAL FINDINGS
Cyanosis
Clubbing of the fingers
Persistent neck vein engorgement
Systolic murmur greater than Gr III/VI

If feasible, women with


some types of severe
cardiac disease should
consider pregnancy
interruption.
If the pregnancy is
continued, prolonged
hospitalization or bed rest
is often necessary.
Anesthesia: epidural
NSD preferred

Diastolic murmur
Predicting Cardiac Complications during Pregnancy

Sustained arrhythmia
Persistently split S2
Loud P2 (criteria for pulmonary hypertension)

Prior heart failure, transient ischemic attack, arrhythmia, or stroke

Baseline NYHA Class III or greater or cyanosis

Left-sided heart obstruction defined as mitral valve area below 2


cm2, aortic valve area below 1.5 cm2, or peak ventricular outflow
tract gradient above 30 mm Hg by echocardiography

Ejection fraction less than 40%

New York Heart Association Classification


Class I

Class II

Class
III

Uncompromised, with no
limitation of cardiac activity.
No symptoms of cardiac
insufficiency or anginal
pain.
These patients usually go
through pregnancy well .
But should still watch out for
any complication which may
push them into failure.
Slightly compromised, with
slight limitation of physical
activity. Comfortable at rest,
but with ordinary or usual
physical activity, the patient
experiences excessive
fatigue, palpitation, dyspnea
or anginal pain.
Management is the same as
that for Class I, but more
vigilance in watching out for
complications is made
because of the higher
incidence of complications.

Markedly compromised,
with marked limitation of
physical
activity.Comfortable at rest
but symptomatic with less
than ordinary activity.
These patients must be comanaged with an internist-

Management
Avoid contact with persons
who have respiratory
infections
Pneumococcal and influenza
vaccines
Cigarette smoking is
prohibited
NSD preferred
During labor, kept in
semirecumbent position
with lateral tilt
Epidural analgesia for
NSD minimize
intrapartum CO fluctuations
and allows forceps or
vacuum assited delivery
CS: epidural anesthesia
SE conduction analgesia:
maternal hypotension
Tubal sterilization and
contraception best after
vaginal delivery and woman
is stable, afebrile, not
anemic, ambuates normally
Management
Impt question whether
pregnancy should be
undertaken
If women make that choice,
they must understand the
risks and cooperate fully
with planned care.

most important predictors of complications were prior


congestive heart failure, depressed ejection fraction,
and smoking
(Williams Obstetrics 23rd edition, 2010)
Signs and Symptoms of Congestive Heart Failure

persistent rales at the lung bases first warning sign of CHF

sudden diminution of the capacity to work

increasing dyspnea on exertion

hemoptysis (usually associated with pulmonary hypertension)

progressive dyspnea, edema and tachycardia

Presence of any of these symptoms warrants


admission. Much of the load on patients occurs at
around the second half of pregnancy

Table 2: ACOG Classification of Risks for Maternal Mortality Caused by


Various Types of Heart Disease
Group 1
Minimal Risk
0-1 %
Atrial septal defect
Ventricular septal defect
Patent ductus arteriosus
Pulmonic or tricuspid disease
Corrected tetralogy of fallot
Bioprosthetic valve
Mitral stenosis, NYHA Class I and II

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Cardiomegaly

Group 2A

Group 2B

Group 3

Moderate Risk
Mitral stenosis, NYHA class III and IV
Aortic stenosis
Aortic coartation without valvular involvement
Fallot tetralogy, uncorrected
Previous myocardial infarction
Marfan syndrome, normal aorta
Moderate Risk
Mitral stenosis with atrial fibrillation
Artificial valve
Major Risk
Pulmonary hypertension
Aortic coarctation with valvular involvement
Marfan syndrome with aortic involvement

5-15%

Patients (ideally) should undergo surgical correction prior to


pregnancy

Features :

5-15%

25-50%

Mitral Stenosis

fixed CO ,

shortened diastolic filling time,

elevated left atrial and

pulmonary capillary pressure

Management

Limit activity + diuretic therapy + dietary sodium restricted

(+) atrial enlargement : anticoagulation is indicated

Valvuloplasty or valve replacement may be necessary if medical


therapy fails

During Labor and Delivery :

Rheumatoid endocarditis causes of mitral stenosis

Contracted valve impedes blood flow from the left atrium to the
right ventricle

8% develop congestion,

6 % experience symptomatic atrial arrhythmia

1-2% may have embolism.

About less than half develop pulmonary hypertension, which is a


poor prognostic factor

invasive hemodynamic monitoring may be helpful

Epidural anesthesia, control of HR , supplemental O2 , semifowlers positioning , avoidance of Valsalva , and assisted forceps
delivery are advisable.

Puerperium : most hazardous time

May need diuretics to prevent pulmonary edema

Aortic Stenosis

1.

Non-responsive pulmonary edema

2.

History of pulmonary edema, even with good medical treatment

3.

Profuse and profound hemoptysis

disease of aging, and in women younger than 30 years, it is most


likely due to a congenital lesion

Uncommon during pregnancy

Stenosis reduces the normal 2- to 3-cm2 aortic orifice and creates


resistance to ejection

Features :
1.

Most common RHD in pregnant patients

Primary symptom : Easy fatigability

Fixed Stroke Volume assoc with stenosis


Exertion may result to dec. O2 delivery to the cerebral
and coronary vessels

2. LV Hypertrophy : compensatory
increases O2 needs of the myocardium

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Indications for surgical treatment:

Pregnancy is contraindicated if valve area is < 1cm2

Goal of mgt : reduce LV afterload

(+) Angina , dyspnea , and syncope :

Epidural anesthesia : recommended

5 yr mortality rate ~ 50%

Management

asymptomatic woman with aortic stenosis, no treatment except


close observation is required

strict limitation of activity and prompt treatment of infections

key to mgt: avoidance of decreased ventricular preload and


maintenance of CO

during L&D: managed on the wet side maintaining a margin


of safety in intravascular volume in anticipation of possible
hemorrage

Avoid tachycardia , maintain filling pressures , prevent decreased


CO and pulmonary edema

Regional anesthesia : use with extreme caution

Valve replacement , valvulotomy , or balloon valvuloplasty may be


necessary

Atrial Regurgitation/ Insufficiency

diastolic flow of blood from the aorta into the left ventricle

Causes: RF, connective-tissue abnormalities, congenital lesions

With Marfan Syndrome aortic root may dilate, resulting in


regurgutation

Aortic and mitral valve insufficiency have been linked to the


appetite suppressants fenfluramine and dexfenfluramine and to
ergot-derived dopamine agonists

Rarely causes LV failure until the 4th or 5th decade of life

Complicates pregnancy in <10% of cases

Mitral Regurgitation/ Insufficiency

Mgt Goals : reduction in afterload

improper coaptation of mitral valve leaflets during systole, some


degree of mitral regurgitation develops followed by left
ventricular dilatation and eccentric hypertrophy
Chronic mitral regurgitation causes
rheumatic fever,
mitral valve prolapse,
or left ventricular dilatation of any etiologyfor
example, dilated cardiomyopathy
Less common causes include a calcified mitral annulus,
possibly some appetite suppressants, and in
older
women, ischemic
heart disease
Mitral valve vegetationsLibman-Sacks endocarditiscommon in
women with antiphospholipid antibodies

Acute mitral insufficiency caused by rupture of a


chorda tendineae, infarction of papillary muscle, or
leaflet perforation from infective endocarditis

Mitral valve prolapse. , Rheumatic fever , or aortic flow


obstruction

Reduced ventricular output = fatigue and dyspnea

Atrial enlargement may lead to AF in long-standing cases

restrict activity

(+) Heart failure : digoxin + diuretics

Epidural anesthesia : recommended

Bradycardia inc. regurgitation across the valve and is poorly


tolerated.

Bacterial endocarditis prophylaxis may be recommended

Pulmonic Stenosis

usually congenital and also may be associated with Fallot


tetralogy or Noonan syndrome

Noonan Syndome - autosomal dominant congenital


disorderconsidered to be a type of dwarfism, that
affects both males and females equally.

principal features include congenital heart


defect (typically pulmonary valve stenosis), short
stature, learning problems, pectus excavatum,
impaired blood clotting, and a characteristic
configuration of facial features including a webbed
neck and a flat nose bridge
Dx: identified by auscultating a systolic ejection murmur over the
pulmonary area that is louder during inspiration.

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Congenital Heart Disease

ASD - atrial septal defects, without pulmonary hypertension

VSD - ventricular septal defects, without pulmonary hypertension


or left-to-right shunts

PDA - patent ductus arteriosus which was corrected in childhood.


If it is not corrected, or if it is with a large left-to-right shunt,
pregnancy can result in left ventricular overload and failure

Pulmonary and Tricuspid valvular lesions, unless, severely


compromised predating pregnancy

Two most common congenital problems are VSD and ASD

Both are abnormal holes in the wall between the side of the heart
that pumps oxygen-poor blood to the lungs, and the side that
pumps oxygen-rich blood out to the body.

Complication occurs if with pulmonary hypertension

Supplemental O2 + measures to inc. vascular resistance + invasive


hemodynamic monitoring

ATRIAL SEPTAL DEFECTS (ASD) :

Common in adults

Most common form : Ostium secundum defect

asymptomatic until the third or fourth decade

Assoc. with mitral valve prolapse or regurgitation

R sided failure and arrhythmias : 4th or 5th decade of life

potential to shunt blood right to left makes possible a paradoxical


embolismentry of a venous thrombus through the septal defect
and into the systemic circulation embolic stroke

Management:

VENTRICULAR SEPTAL DEFECT (VSD)

During pregnancy : well tolerated and requires no specific therapy


in most gravidas

Invasive monitoring : rarely needed

Epidural anesthesia : preferred

Compression stockings+prophylactic heparin in othe presence of


immobility

Bacterial endocarditis prophylaxis

ATRIOVENTRICULAR SEPTAL DEFECT

Small VSDs : well tolerated

if the defect is less than 1.25 cm2, pulmonary hypertension and


heart failure do not develop

(+) L to R shunting inc. pulmonary vascular resistance reverse


shunting with cyanosis occurs

When pulmonary arterial pressures reach systemic levels,


however, there is reversal or bidirectional flowEisenmenger
syndrome (Eisenmenger syndrome)

Epidural anesthesia : may not be tolerated

During labor : if cyanosis develops = R to L shunting

characterized by a common, ovoid-shaped AV junction


associated with aneuploidy, Eisenmenger syndrome, and other
malformations, some of these women become pregnant

PATENT DUCTUS ARTERIOSUS (PDA) :

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Shunts blood from high pressure aorta to the lower pressure


pulmonary artery

Usually corrected during childhood

Small PDAs : well tolerated in pregnancy

Benign course until middle ages

Usually corrected during infancy

Clinical : BP gradient between upper and lower extremity

Isolated HPN in the R upper arm

Fixed stroke volume

Cerebral berry aneurysms : common

Patients with prior repair should be reevaluated for aortic


narrowing

TETRALOGY OF FALLOT (TOF) :

DEVELOPMENTAL CARDIAC LESIONS


EISENMENGERS SYNDROME :

a. RV outflow obstruction
b. VSD
c. RV hypertrophy
d. Aorta overriding the VSD
R to L shunting : usually present

Uncorrected lesions :

reduced life expectancy


Pregnancy is rare
If (+) pregnancy =spontaneous abortion , IUGR , cardiac
failure

Corrected lesions :

Pregnancy : well tolerated


Inc. risk of IUGR

During Labor and Delivery :

Supplemental O2 + efforts to maintain venous return


Narcotics or pudendal block : vaginal delivery
General anesthesia : CS delivery
Vaginal delivery preferred

COARCTATION OF THE AORTA :

secondary pulmonary hypertension that develops from any cardiac


lesion

R to L shunt (via ASD , VSD , or PDA) underlying defects

elevated pulmonary vascular resistance

Maternal (12-70%) and fetal (50%) mortality are high

Cyanosis ,chest pain , syncope , and hemoptysis :


prognosis

Termination of pregnancy is an option

For patients who continue with pregnancy : limit activity ,


anticoagulation , maintenance of preload , supplemental O2 ,
avoid hypovolemia

poor

PULMONARY HYPERTENSION

N resting mean pulmonary artery pressure 12-16mmHg


a hemodynamic observation and not a diagnosisis defined in
nonpregnant individuals as a mean pulmonary pressure >25 mm
Hg
Class I indicates a specific disease that affects pulmonary
arterioles. It includes idiopathic or "primary" pulmonary
hypertension as well as those cases secondary to a known cause
such as connective-tissue disease
Class II disorders are more commonly encountered in pregnant
women caused by left-sided atrial, ventricular or valvular
disorders

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Clinical Classification of Some Causes of Pulmonary Hypertension in


Pregnancy
I. Pulmonary arterial
Idiopathic primary pulmonary HPN
hypertension
Familial eg. Chromosome 2 gene in TGF
superfamily
Assoc with: collagen vascular disease,
congenital left-to-right shunts, HIV infection,
thyrotoxicosis, sickle cell hemoglobinopathis,
APAS, portal HPN
Persistent pulmonary HPN in newborn
other
II. Pulmonary
Left-sided atrial or ventricular disease
hypertension with

Left-sided valvular disease


left-sided heart
disease
III. Pulmonary
Chronic obstructive pulmonary disease
hypertension

Interstitial lung disease


associated with lung

Other
disease
IV. Pulmonary
hypertension due to
chronic
thromboembolic
disease
V. Miscellaneous
Diagnosis
S/Sx: vague, dyspnea with exertion (most common)
Class II: orthopnea, nocturnal dyspnea
Angina and syncope when right ventricular output is fixed
Chest radiography shows enlarged pulmonary hilar arteries and
attenuated peripheral markings; disclose parenchymal causes of
hypertension
Diagnosis is by echocardiography and is confirmed by right-sided
catheterization, which usually may be deferred during pregnancy
Pulmonary Hypertension and Pregnancy

Idiopathic- worst prognosis


Pregnancy is contraindicated with severe disease, especially those
with pulmonary arterial changesmost class I. With milder
degrees of other causesclass II being commonthe prognosis is
much better

MARFANS SYNDROME :

(+) dilated aortic root prior to pregnancy : maternal


mortality ~50% during pregnancy
Aortic root diameter >40mm : risk of aortic dissection
If 50-60 mm elective surgery before
pregnancy
Aortic dilatation and dissecting aneurysm are the most
serious abnormalities

Management :

prevent HPN
Beta blockers
Regional anesthesia : well tolerated

MITRAL VALVE PROLAPSE :

Dx: presence of a pathological connective tissue disorderoften


termed myxomatous degenerationwhich may involve the valve
leaflets themselves, the annulus, or the chordae tendineae

Most common cardiac lesion in women

Incidence : ~ 12%

Most patients are asymptomatic and have uneventful pregnancies

B-blockers - given to decrease sympathetic tone, relieve chest pain


and palpitations, and reduce the risk of life-threatening
arrhythmias

Endocarditis prophylaxis is not indicated unless there is a


coexistent mitral insufficiency

Autosomal dominant genetic disorder with high dregree of


penetrance
caused by abnormal fibrillina constituent of elastincaused by
any of dozens of mutations in the FBN1 gene located on
chromosome 15q21

Coronary Artery Disease

Peripartal Cardiomyopathy

cardiomegaly

presence of S3

jugular
distention

mitral or
tricuspid
regurgitation

diastolic or late systolic murmurs

cool extremities

Weakened connective tissue

Cardiac manifestation : weakness of aortic root and


mitral valve prolapse

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Other Cardiac Conditions

Timing of Delivery

diagnosis of exclusion following a


contemporaneous cardiac evaluation of
peripartum heart failure
similar to idiopathic dilated
cardiomyopathy encountered in
nonpregnant adults

Current NYHA functional status (hemodynamic compensation)

Fetal compromise (fetal growth restriction

Oligohydramnios or nonreassuring fetal tracing

Functional status trend over time

Possibility of improving or relieving the current functional status


through optimization of treatment

Diagnostic Criteria
1.
2.
3.
4.

Development of heart failure in the last month of pregnancy or


within 5 months after delivery.
Absence of an identifiable cause for the heart failure.
Absence of recognizable heart disease prior to the last month of
pregnancy.
Left ventricular dysfunction demonstrated by 2D Echo
such as depressed ejection fraction

evaluation of compliance

adjustment of medication doses or additional


medications

additional rest
(Gei, 2001)

Idiopathic Cardiomyopathy in Pregnancy

After exclusion of an underlying cause for heart failure, the default


diagnosis is idiopathic or peripartum cardiomyopathy
Women with cardiomyopathy present with signs and symptoms of
congestive heart failure.
Dyspnea is universal, and other symptoms include orthopnea,
cough, palpitations, and chest pain
hallmark finding usually is impressive cardiomegaly

Hypertrophic Cardiomyopathy

Concentric left ventricular hypertrophy may be familial, and there


also is a sporadic form not related to hypertension, termed
idiopathic hypertrophic subaortic stenosis
Characterized by: cardiac hypertrophy, myocyte disarray, and
interstitial fibrosisis caused by mutations in any one of more
than a dozen genes that encode proteins of the cardiac sarcomere
autosomal dominant
abnormality is in the myocardial muscle, and it is characterized by
left ventricular myocardial hypertrophy with a pressure gradient
to left ventricular outflow
Dx: established by echocardiographic identification of a
hypertrophied and nondilated left ventricle in the absence of other
cardiovascular conditions
Management:
Strenuous exercise prohibited during pregnancy
Abrupt positional changes are avoided to prevent reflex
vasodilation and decreased preload
B adrenergic/Ca channel given if symptoms develop
like angina
Spinal analgesia - contraindicated

Management Principles during Delivery

Relief of pain

Outlet forceps delivery to avoid the Valsalva maneuver

Available blood for transfusion

Prophylactic antibiotics (for valvular problems)

Maintain patients in Fowlers and semi-recumbent position

Maintain on continuous oxygen inhalation

Infective Endocarditis

General Principles of Antenatal Management


1.
2.
3.

4.
5.

All pregnant patients with heart disease should be asked to limit


their physical activities based on classification.
Sexual activity is not contraindicated in patients in Class II.
A high protein, low salt (2 gms/day) has been recommended by
some authorities but the low sodium recommendation have not
been shown to be useful except, in severe cases of congestive
heart failure in the hospital setting and in those on diuretics for
their predisposition to hypokalemia.
Routine supplementation with folic acid and iron sulfate is
recommended as tolerated.
Anticoagulant drugs may be needed in pregnancy because of
recurrent deep vein thrombosis, pulmonary embolism, rheumatic
heart disease with atrial fibrillation, prosthetic valves or cyanotic
congenital heart disease.

infection involves cardiac endothelium and produces vegetations


that usually deposit on a valve
Subacute bacterial endocarditis due to a low-virulence
bacterial infection superimposed on an underlying structural lesion
most common causative organisms are streptococciespecially
viridansfollowed by Staphylococcus aureus and Enterococcus
IV drug abusers S. aureus is the predominant organism.
Staphylococcus epidermidis commonly causes prosthetic valve
infections
Streptococcus pneumoniae and Neisseria gonorrhoeae cause
acute, fulminating disease
Antepartum endocarditis has been described with Neisseria sicca
and Neisseria mucosa, the latter causing maternal death
Dx: fever, murmur, Anorexia, fatigue, and other constitutional
symptoms are common, and the illness is frequently described as
"flulike
embolic lesions, including petechiae, focal neurological
manifestations, chest or abdominal pain, and ischemia
in an extremity
Mgt:
Most viridans streptococci are sensitive to penicillin G
given intravenously with gentamicin for 2 weeks
women allergic to penicillin are either desensitized or
given intravenous ceftriaxone or vancomycin for 4
weeks
Staphylococci, enterococci, and other organisms are
treated according to microbial sensitivity for 4 to 6
weeks
Prosthetic valve infections are treated for 6 to 8 weeks
Right-sided infections caused by methicillin-resistant S.
aureus (MRSA) vancomycin

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Peripartum Cardiomyopathy

Endocarditis Prophylaxis

2 gms Ampicillin and 1.5mg/kg Gentamicin, 30 mins. prior to the


procedure, followed by 1 gm of Ampicillin as a second dose

High Risk Patients

1.
2.
3.
4.

Moderate Risk
Category

1.
2.
3.

Prosthetic cardiac valves (bioprosthetic and


homograft)
Previous bacterial endocarditis
Complex cyanotic congenital heart disease
(Fallot or TGA)
Surgically corrected systemic pulmonary
shunts or conduits
Other congenital heart disease
Acquired valvular dysfunction
MVP with regurgitation or thickened
leaflets

Negligible Risk

Management Principles during Post-Partum Period

Maintain on hospital confinement for at least another week

Avoid extra exertion, maintain on bed rest

Massage uterus to avoid atony

Note : Italicized words were lifted from the book. Cardiac arrthymias and
ischemic heart diseases were not included in the trans.
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References:

Cunningham et al. Williams Obstetrics: 23rd ed, chap44. McGraw


Hill Publishing. 2010.
Dra Pascuals lec

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That in all Things, God may be Glorified

Transcribed by: Ice A Soria

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