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OBSTETRICS 2

Cardiovascular
3S-2 | CEU-SOM A & B
ELEYNETH I. VALENCIA, MD, FPOGS, FPSUOG
Disorders

OUTLINE Ø At 30-32 weeks: repeat CBC to check if maternal iron supplement
is sufficient
I. CARDIOVASCULAR PHYSIOLOGY Ø If with heart disease: the heart cannot always accommodate these
II. DIAGNOSIS OF HEART DISEASE changes
III. PERIPARTUM MANAGEMENT CONSIDERATIONS Ø Ventricular dysfunction leads to cardiogenic heart failure
IV. SURGICALLY CORRECTED HEART DISEASE Ø In most, HEART FAILURE develops PERIPARTUM
V. VALVULAR HEART DISEASE o In labor
VI. CONGENITAL HEART DISEASE o During delivery
VII. PULMONARY HYPERTENSION o (+) several obstetric conditions that may add burden e.g.,
VIII. CARDIOMYOPATHIES preeclampsia, hemorrhage, anemia, and sepsis
IX. HEART FAILURE
X. INFECTIVE ENDOCARDITIS U One of the recommendations of the Society of Maternal and Fetal
XI. ISCHEMIC HEART DISEASE Medicine, patients with cardiovascular disease should stay in the
XII. REFERENCE hospital for at least 10 days postpartum.
XIII. APPENDIX
EFFECT OF PREGNANCY ON HEART DISEASE
MATERNAL MORTALITY
Worsening Cardiac Status: decomposition (heart failure)
Ø Between 2011 to 2013: previously responsible for maternal deaths
– declining Ø During pregnancy: increase CO at 28-32 weeks
Ø Hemorrhage Ø During labor: due to stress of labor
Ø Hypertensive Disorders Ø After delivery: the most dangerous period due to sudden return of
Ø Embolism the blood to the general circulation
Ø Cardiovascular disorders: 26% of pregnancy related deaths
VENTRICULAR FUNCTION IN PREGNANCY
Prevalence
Ø ↑ end systolic and systolic dimensions
Ø Rising prevalence is due to: Ø Septal thickness/Ejection Fraction are unchanged
Ø Obesity Ø Ventricular remodeling – plasticity (eccentric expansion of the L.
Ø Hypertension ventricular mass – 30-35% near term)
Ø Diabetes
Ø National Center for Health Statistics & Remodeling will return to its pre-pregnancy values usually on the
Ø Almost ½ of adults aged ≥20 – at least 1 risk factor 6th to 12th weeks postpartum
Ø Delayed childbearing
II. DIAGNOSIS OF HEART DISEASE
I. CARDIOVASCULAR PHYSIOLOGY
Physiological adaptations of normal pregnancy
Marked Pregnancy-Induced Anatomical and Functional Changes in o Induce symptoms
Cardiac Physiology → profound effect on underlying heart disease o Alter clinical findings
o Confound the diagnosis of heart disease
1. Cardiac Output: increased 40% (at term; ½ of total by 8 weeks
and max by midpregnancy) Normal pregnancy
2. ↑ Stroke Volume o Functional systolic heart murmur common
3. ↓ Vascular resistance o Accentuated respiratory effort
4. ↑ Resting pulse and SV due to ↑ EDV from pregnancy o Lower extremity edema after midpregnancy
hypervolemia o Fatigue and exercise intolerance

VARIABLE CHANGE NORMAL PREGNANCY INDICATORS OF


Cardiac Output Increased by 30-50% ISCHEMIC HEART DISEASE
Strove Volume Increases to a maximum of 85 mL at 20 weeks of Mild dyspnea Severe or progressive dyspnea
gestation Fatiguability Syncope with exertion
Heart rate Increased (approaches 90-100 bpm at rest during the Decreased exercise tolerance Chest pain with effort of emotion
3rd trimester Chest pain at rest
Systemic Decrease 21% (nadir at 14-24 weeks; around 1200 Table 2. Indicators of Ischemic Heart Disease
Vascular dyne/s/cm5)
Resistance Clinical indicators of heart disease during pregnancy
Pulmonary Decrease by 34% to a nadir of 78 dyne/s/cm5
Vascular
Ø Symptoms
Resistance o Progressive dyspnea or orthopnea
Pulmonary No significant change o Nocturnal cough, hemoptysis, syncope, chest pain
Capillary
Wedge Ø Clinical findings
Pressure Ø Cyanosis, clubbing of fingers
Colloid Decreased by 14% (associated with a decrease in Ø Persistent neck vein distension
Osmotic serum osmolarity noticed as early as first trimester of Ø Systolic murmur grade 3/6 or greater
Pressure pregnancy)
Ø Diastolic murmur, cardiomegaly
Hemoglobin Decreased (maximum hemodilution is achieved at 30-
Concentration 32 weeks) Ø Persistent arrythmia
Table 1. Physiologic changes during pregnancy Ø Persistent split – second sound
Ø Criteria for pulmonary hypertension
3S-2 CARDIOVASCULAR DISORDERS ESTUYE • HO • JAVIER • PASAJOL • RAMOS • ROCHA
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DIAGNOSTIC STUDIES

Noninvasive cardiovascular studies such as electrocardiography, chest


radiography, and echocardiography will provide data necessary for
evaluation

Normal Diagnostic Studies

Ø ECG
o Average of 15º left axis deviation – diaphragm is elevated in
advancing pregnancy
o Reduced PR interval
o Inverted or flattened T waves
o Voltage findings not altered
o Atrial and ventricular premature contractions – relatively
frequent

Ø Chest X-ray
o AP and lateral views
o Must use lead apron shield – fetal radiation exposure –
minimal
o Slight heart enlargement – not detected accurately due to
heart silhouette larger in pregnancy Table 4. WHO risk classifIcation of CVD & pregnancy

Ø Echocardiography (2D-echo) PRECONCEPTIONAL COUNSELLING


o Widely used; permits accurate diagnosis of most heart
diseases Ø Most especially beneficial for patients with SEVERE heart disease
o Some normal pregnancy-induced changes: Ø Referred for Maternal-Fetal Medicine or Cardio Consult
§ Small increase in dimensions of the cardiac chambers Ø Must identify life threatening cardiac abnormalities
§ Slight growth in the left ventricular mass Ø Fetal teratogenic concerns
§ Tricuspid and mitral valve regurgitation Ø Issues on congenital heart lesions

Ø Cardiovascular MRI III. PERIPARTUM MANAGEMENT CONSIDERATIONS


o With higher reproducibility
o Less hindered by ventricular geometry and body habitus Ø Team approach: OB, Cardiologist, Anesthesiologist and other
o classification of functional heart disease specialties as needed
Ø Prognosis and Management: Influenced by the TYPE and
SEVERITY of lesions and MATERNAL FUNCTIONAL
CLASSIFICATION
Ø NYHA Class I and most in NYHA Class II – may negotiate
pregnancy without morbidity
§ If III and IV: pregnancy is contraindicated
Ø To prevent or to early recognize HF
Ø Identify infection or sepsis syndrome that can precipitate HF
Ø To avoid contact with respiratory infections
Ø Pneumococcal and influenza vaccines recommended
Ø Cigarette smoking prohibited
Ø Illicit drug use is prohibited
Ø peripartum management
CLASSIFICATION OF FUNCTIONAL HEART DISEASE Ø NYHA Class III and IV are UNCOMMON
Ø If a woman chooses pregnancy: MUST understand the risk and
must be encouraged to be compliant with PLANNED CARE
§ (+) prolonged hospitalization or bed rest is often
necessary with continued plan of care

Table 3. Clinical classification of the New York Heart Association based on the
past and present disability uninfluenced by physical signs

Space Filler

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LABOR AND DELIVERY Ø Over-all estimated maternal mortality rate: 1.2
Ø Pregnancy FREE of SERIOUS complications:
Ø In general o Mechanical: 58%; increased risk of thrombosis
o Vaginal Delivery is preferred o Tissue Heart Valve: 79%
o Labor induction is usually safe o Porcine Tissue Valves: safer; anticoagulation not required;
Ø Planned CS conferred NO ADVANTAGE for maternal or neonatal less durable; longevity average 10-15 years
outcome
o Limited to obstetrical indications Anticoagulation
o For specific cardiac lesions
o Over all maternal condition Ø Critical for women with mechanical prosthetic valves
o Availability of experience, Anesthesia personnel and hospital Ø Warfarin – risk HIGH: mean daily dose >5 mg; embryopathy >8%
capabilities o Most effective anticoagulant for preventing maternal
Ø Mother in labor – kept in semi-recumbent position (left lateral) thromboembolism
with lateral tilt o Teratogenic, causes miscarriage, still births
Ø VS taken frequently between contractions Ø Heparin – is less hazardous for fetus – ↑ thromboembolism
Ø Watch out for impending ventricular failure: PR: >100 bpm or
RR >24 cpm Pregnancy after Heart Transplantation
Ø Cesarean Section is recommended:
o Dilated aortic root >4 cm or aortic aneurysm Ø May have successful pregnancies following cardiac
o Acute severe congestive heart failure transplantation
o Recent myocardial infarction Ø International Society of Heart and Lung Transplantation: Don’t
o Severe aortic stenosis discourage pregnancy in stable heart transplant recipients > 1 year
o Warfarin administration within 2 weeks of delivery posttransplant
o Need for emergency valve replacement immediately after
delivery V. VALVULAR HEART DISEASE
RHEUMATIC FEVER
Analgesia and Anesthesia
Ø Uncommon in the US because of:
Ø Relief from pain and apprehension o less crowded living conditions
Ø IV anesthesia: satisfactory relief for pain o penicillin availability
Ø Continuous epidural anesthesia is recommended o evolution of non-rheumatogenic streptococcal strains
Ø Still remains the chief cause of serious mitral valvular disease in
Intrapartum Heart Failure women of childbearing age

Ø Cardiovascular decompensation during labor: MITRAL STENOSIS


o Pulmonary edema (tx with diuresis)
o Hypoxia Ø Rheumatic endocarditis causes most mitral stenosis
o Hypotension Ø For severe stenosis: L atrium dilates, elevated L atrial pressure,
significant passive pulmonary hypertension develops.
PUERPERIUM Ø These women have a relatively fixed CO, thus, the increased
preload of normal pregnancy and other factors that raise CO may
Ø May still decompensate postpartum cause ventricular failure and pulmonary edema
Ø Fluid is mobilized into intravascular compartment Ø (+) dyspnea, fatigue, palpitations, cough, hemoptysis
Ø Reduced peripheral vascular resistance place higher demands
on myocardial performance PREGNANCY OUTCOMES
Ø Worsen heart failure:
o PPH Ø 43% develops heart failure
o Anemia Ø 20% develops arrhythmias
o Infection Ø IUGR common for mitral valve area < 1 cm2
o Thromboembolism Ø Prognosis depends on functional capacity: 8 out of 10 deaths for
Ø Severe preeclampsia may cause or worsen pulmonary edema NYHA Classes III or IV
Ø Puerperal tubal sterilization – after VD – delayed after SEVERAL
DAYS MANAGEMENT
Ø Mother is hemodynamically stable, afebrile, not anemic,
ambulatory Ø Limited physical activities
Ø If with pulmonary congestion: dietary Na restriction + diuretics
IV. SURGICALLY CORRECTED HEART DISEASE Ø Beta-blocker if tachycardic
Ø Surgical intervention: mitral valve area is 1.5-2 cm2
Ø Significant congenital heart lesions – repaired during childhood Ø Ideal for delivery: vaginal delivery under epidural anesthesia
Ø Not diagnosed until adulthood:
o ASD
o Pulmonic stenosis
o Bicuspid Aortic Valve
o Aortic Coarctation
Ø Some are mild and surgery NOT required
Ø If for surgery, IDEALLY performed BEFORE pregnancy

Valve Replacement Before Pregnancy

Ø Prosthetic mitral or aortic valve → may cause MI, anticoagulation


is needed
Ø Type of valve:
o Mechanical
o Biological

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o Symptomatic: strict limitation of activity, treatment of
infection; surgery
MITRAL INSUFFICIENCY

Ø Trivial degree of mitral insufficiency is found in normal patients


Ø If mitral valve leaflets align improperly during systole – abnormal
degrees of mitral regurgitation can develop
Ø Followed by left ventricular dilatation, eccentric hypertrophy
Ø Acute mitral insufficiency is caused by:
o Chordae tendinae rupture
o Papillary muscle infarction
o Leaflet perforation
Ø Chronic mitral regurgitation is caused by:
o Rheumatic fever
o Connective tissue disease
Ø Mitral valve vegetations: Libman-Sacks endocarditis relatively
common in women with antiphospholipid antibodies, sometimes
coexist with SLE
Ø Mitral Regurgitation is tolerated in pregnancy because the lowered
systemic vascular resistance yields less regurgitation AORTIC INSUFFICIENCY
MITRAL VALVE PROLAPSE (MVP) Ø Allows diastolic flow of blood from the aorta back into the LV
Ø Frequent causes:
Ø This diagnosis implies the presence of pathological connective o Rheumatic fever
tissue disorder – myxomatous degeneration – which may involve o Connective tissue abnormalities
the valve leaflets, annulus, chordae tendinae o Congenital lesions
Ø Usually asymptomatic and are diagnosed during routine Ø Acute insufficiency may develop from bacterial endocarditis
examination or echocardiography Ø Symptoms: slow onset fatigue, dyspnea, pulmonary edema
Ø Pregnant women with MVP rarely have cardiac complications Ø Generally well-tolerated during pregnancy due to diminished
Ø For symptomatic women, give beta-blocking agents – decrease vascular resistance (improve hemodynamic function)
sympathetic tone, relieve chest pain and palpitations, and reduce Ø Treatment: diuretics and bed rest (if symptoms of heart failure
risk of life-threatening arrhythmias develops)
Ø Women with symptoms have anxiety, palpitations, atypical chest
pain, dyspnea with exertion and syncope

PULMONARY STENOSIS

Ø Usually congenital and may be associated with Tetralogy of Fallot


or Noonan syndrome.
Ø The greater hemodynamic burden of pregnancy can precipitate
right sided HF or atrial arrhythmias in women with severe stenosis
Ø Surgical correction: ideal before pregnancy

AORTIC STENOSIS VI. CONGENITAL HEART DISEASE

Ø A disease of aging; if in young: congenital lesion Ø Most common type of heart disease encountered in pregnancy
Ø Concentric L ventricle hypertrophy → increase end diastolic Ø Greater maternal mortality rates
pressure → decrease ejection fraction → CO
Ø Manifestations: chest pain, syncope, heart failure, sudden death ATRIAL SEPTAL DEFECT
from arrhythmias
Ø Life expectancy after exertional chest pain develops: 5 years Ø ¼ of all adults has a patent foramen ovale
Ø In pregnancy: mild – mod – well tolerated Ø Most ASDs are asymptomatic until 3rd to 4th decade
Ø Maternal mortality rate: 8% Ø Secundum type defect accounts for 70%, and associated with
Ø Management: mitral valve myxomatous abnormalities with prolapse
o Asymptomatic: no treatment, observe Ø If discovered in childhood → repair
Ø Pregnancy is well tolerated unless pulmonary hypertension has
developed (uncommon)
Ø Treatment of ASD during pregnancy is indicated for congestive
heart failure or an arrhthmia
Ø Right → Left shunt: paradoxical embolism – entry of venous
thrombus through the defect and into the systemic arterial
circulation may cause embolic stroke

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PATENT DUCTUS ARTERIOSUS

Ø The ductus connects the proximal left pulmonary artery to the


ascending aorta just distal to the L subclavian artery
Ø Functional closure from vasoconstriction occurs shortly after birth
Ø If persistent and unrepaired: high mortality after the 5th decade
Ø Pregnancy: develops pulmonary hypertension, heart failure,
cyanosis if systemic blood pressure falls and leads to shunt
reversal of blood from the pulmonary artery into the aorta; sudden
hypotension at delivery after regional anesthesia or hemorrhage
may lead to fatal collapse

VENTRICULAR SEPTAL DEFECT

Ø Close spontaneously during childhood in 90% of cases


Ø Most defects are paramembranous, and the degree of left-to-right
shunt and associated physiological derangements are related to
lesion size
Ø Pulmonary hypertension and heart failure may develop
Ø Ideal: children to undergo surgical repair before pulmonary
hypertension develops
Ø Pregnancy: well-tolerated for small-to-moderate sized shunts
Ø Bacterial endocarditis is more common with unrepaired defects, CYANOTIC HEART DISEASE
and antimicrobial prophylaxis is often required
Ø 10-16% of offspring has VSDs Ø Cyanosis: R to L shunting of blood past pulmonary capillary bed
Ø Most commonly encountered lesion in adults: Tetralogy of Fallot
o Characterized by a large ventricular septal defect,
pulmonary stenosis, RV hypertrophy, and an overriding
aorta that receives blood from both the right and left
ventricles
Ø Do poorly during pregnancy
Ø Maternal mortality rate: 10%
Ø Chronic hypoxemia, polycythemia, miscarriage and perinatal
morbidity
Ø Not all cyanotic lesions are repairable

PREGNANCY AFTER SURGICAL REPAIR

TRANSPOSITION OF THE GREAT VESSELS

Ø Pregnancy following surgical correction of transposition of the great


ATRIOVENTRICULAR SEPTAL DEFECT vessels has prominent risks
Ø 3% of all congenital cardiac anomalies are AVSD SINGLE FUNCTIONAL VENTRICLE
Ø AV septal defect is characterized by a common, ovoid AV junction.
Ø This defect is associated with aneuploidy, Eisenmenger syndrome,
other malformations Ø Hypoplastic left heart syndrome – 70% survived ADULTHOOD
Ø Compared with simple septal defects, complications are more Ø Cardiac arrhythmias, thromboembolism
frequent during pregnancy.
Ø Identified in 15% of offspring EISENMENGER SYNDROME

Ø Secondary pulmonary hypertension that arises from any cardiac


lesion
Ø Develops when pulmonary vascular resistance exceeds systemic
resistance and leads to concomitant right-to-left shunting
Ø Pregnant women with this syndrome tolerate hypotension poorly,
and death usually is caused by right ventricular failure with
cardiogenic shock
Ø Given such poor outcomes for both the mother and the fetus,
Eisenmenger syndrome is considered to be an ABSOLUTE
CONTRAINDICATION to pregnancy

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DIAGNOSIS

Ø Hypertrophied heart, non-dilated left ventricle in the absence of


other CV conditions
Ø Asymptomatic: may have with dyspnea, angina, or atypical chest
pain, syncope, arrhythmias
Ø Symptoms worsen with exercise; ventricular tachycardia ® death

MANAGEMENT

Ø Avoid strenuous exercise, abrupt positional changes


Ø Delivery route: OB indications
Ø Choice of anes: controversial

SEE APPENDIX
DILATED CARDIOMYOPATHY

Ø Left or right ventricular enlargement


VII. PULMONARY HYPERTENSION
Ø Reduced systolic function in the absence of coronary, valvular,
congenital or systemic diseases causing myocardial dysfunction
Ø Normal resting mean pulmonary artery pressure is 12 to 16 mmHg.
Ø Both inherited and acquired (viral infection: myocarditis or HIV)
Ø Pulmonary hypertension is defined in nonpregnant individuals as a
Ø Potentially reversible if causes: alcoholism, cocaine abuse, thyroid
resting mean pulmonary pressure > 25 mmHg
disease
Ø Pregnant: Group 2 disorders are the most common – secondary to
pulmonary venous hypertension caused by L-sided atrial,
PERIPARTUM CARDIOMYOPATHY
ventricular or valvular disorders
Ø Non-ischemic dilated CM
(See appendix for comprehensive clinical classification of pulmo HTN)
Ø Unique relationship with pregnancy
Ø Shares genetic predisposition
DIAGNOSIS
Ø Etiology: remains unknown
Ø Oxidative stress during late pregnancy: proteolytic cleavage of
Ø Vague symptoms, dyspnea with exertion is the most frequent prolactin ® 16-kDa prolactin fragment: cardiotoxic and impair
Ø For group 2 disorders: orthopnea, nocturnal dyspnea cardiomyocyte metabolism and contractility
Ø Angina and syncope occur when right ventricular output is fixed and
they suggest advanced disease DIAGNOSIS OF EXCLUSION
Ø Chest radiography: enlarged pulmonary hilar arteries and
attenuated peripheral markings
Ø With the following Diagnostic Criteria:
PROGNOSIS • Development of heart failure in the last month of pregnancy or
within 5 months postpartum
• Absence of an identifiable cause of heart failure
Ø Regardless of etiology, the final common pathway of pulmonary
• Absence of recognizable heart disease before the last month
hypertension is right heart failure and death (<4 years)
of pregnancy
Ø Pregnancy contraindicated: with severe disease
• Left ventricular systolic dysfunction demonstrated by left
ventricular ejection fraction of less than45%, fractional
MANAGEMENT
shortening of less than 30%, or both, with or without a left
ventricle end-diastolic dimension less than 2.7 cm/m2 of body
Ø Activity limitation surface area
Ø Avoidance of supine position later in gestation
Ø Standard treatment: Diuretics; supplemental 02; pulmonary PROGNOSIS
vasodilator drugs
Ø During labor and Delivery:
Ø >1/2 recover baseline recovery within 6 months of delivery
o These women are at greatest risk when venous return
Ø If with persistent cardiac failure: 85% mortality rate (5 years)
and right ventricular filling are diminished
o To avoid hypotension, assiduous attention is given to
SUBSEQUENT PREGNANCY
epidural analgesia induction and to blood loss prevention
and treatment at delivery.
Ø may suffer relapse with worsening of symptoms
Ø 20% of women at risk for deterioration in left ventricular function
VIII. CARDIOMYOPATHIES
IX. HEART FAILURE
Ø Heterogenous group of myocardial disease with mechanical and/or
electrical dysfunction (American Heart Association) Ø Pre-existing heart ds + PES = 30% risk of heart failure
Ø Primary Cardiomyopathy – solely or predominantly confined to Ø ­ with infection and sepsis - ­ carbon dioxide and oxygen utilization
heart muscle, e.g., hypertrophic CM, dilated CM, peripartum CM and depress myocardial function
Ø Secondary Cardiomyopathy – result from generalized systemic
disorders that produce pathological myocardial involvement, e.g., SYMPTOMS
DM, SLE, CHVD, thyroid disorder
Ø Gradual onset or acute pulmonary edema on 3rd trimester
HYPERTROPHIC CARDIOMYOPATHY Ø Dyspnea
Ø Orthopnea
Ø Cardiac hypertrophy, myocyte disarray, interstitial fibrosis Ø Palpitations
Ø Inheritance is autosomal dominant Ø Substernal chest pain
Ø Left ventricular myocardial hypertrophy with pulmonary gradient vs Ø Decline in the performance of duty
left ventricular outflow Ø Nocturnal cough

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CLINICAL FINDINGS TREATMENT

Ø Persistent bibasilar rales Ø Primarily medical


Ø Hemoptysis Ø Ascertain infecting organism
Ø Progressive enema
Ø Tachypnea PREGNANCY
Ø Tachycardia
Ø Uncommon even in puerperium
HALLMARK RADIOLOGIC FINDINGS Ø (+) heart valve problems: given Endocarditis prophylaxis

Ø Cardiomegaly
Ø Pulmonary edema PROPHYLAXIS

ECHOCARDIOGRAPHY Ø American Heart Association (AHA)


• According to AHA, patients for whom dental prophylaxis is
Ø EF < 0.45 recommended:
Ø Fractional shortening <30% o Only those at highest risk, i.e., those with:
Ø End diastolic dimension >2.7 cm/m2 § a prosthetic cardiac valve
§ a history of infective endocarditis
MANAGEMENT § certain forms of congenital heart disease
§ unrepaired cyanotic congenital heart disease,
Ø Pulmonary edema – responds to diuretics to reduce preload including palliative shunts and conduits
Ø Hypertension – hydralazine and other vasodilator to reduce § completely repaired congenital heart disease
afterload with prosthetic material or device during the
Ø Left ventricular assist device first 6 months after the procedure
Ø ECMO – extracorporeal membrane oxygenation – life-saving if with § repaired congenital heart disease with residual
fulminating CM and pulmonary HPN defects at the site or adjacent to the site of
prosthetic patch or prosthetic device
X. INFECTIVE ENDOCARDITIS § valvulopathy after cardiac transplantation

Ø Greatest risk: (+) CHD • AHA recommends prophylaxis:


Ø Sub-Acute Endocarditis o does not recommend endocarditis prophylaxis for
o Low virulence bacterial infection + underlying structural either vaginal or CS delivery in the absence of
lesion pelvic infection except with the lesion cited by AHA
Ø Viridans-group streptococcus o given for women at risk for endocarditis (cyanotic
Ø Staphylococcus heart disease, prosthetic valves, or both)
Ø Enterococcus
Ø IV drug abusers/ catheter related infection: Staphylococcus aureus Ø American College of Obstetrics and Gynecologists (ACOG,
Ø Prosthetic valves: Staphylococcus epidermidis 2016)
Ø Fulminating disease: Streptococcus pneumoniae and Neisseria • Administer 30-60 minutes prior to the anticipate delivery
gonorrhea • Standard (IV): Ampicillin 2g or Cefazolin or Ceftriaxone 1g
• Penicillin-allergic (IV): Cefazolin or Ceftriaxone 1g or
DIAGNOSIS Clindamycin 600mg
• Oral: Amoxicillin 2g
Ø Fever with chills – 80-90%
Ø Murmur – 85% XIII. ISCHEMIC HEART DISEASE
Ø Anorexia, fatigue and constitutional symptoms

CLINICAL CLUES Ø Mortality rate is higher compared to non-pregnant woman


Ø If sustained <2 weeks before delivery: high risk for death due
to greater demand of labor and delivery
Ø Anemia
Ø Proteinuria
Ø Diagnosis
Ø Manifestations of embolic lesions: petechiae, focal neurological
o It does not differ in non-pregnant woman which
changes, chest and abdominal pain, ischemia in extremity
include:
Ø Symptoms of heart failure
§ Characteristic ECG changes
§ Evidence of myocardial necrosis –
elevated Troponin levels
§ High index of suspicion: (+) chest pain
o Coronary Angiography – diagnostic standard

Ø Treatment
o Similar to non-pregnant woman
CS reserved for obstetrical indications or epidural anesthesia id

XIV.REFERENCES

Ø Williams Obstetrics, 25th Edition (Cunningham et al)


Ø Dr. Valencia’s PPT
Ø Notes and Recordings of OB2 Trans Team

“Vitanda est improba siren desidia. (One must avoid that


wicked temptress, Laziness.)”― Horace

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XV.APPENDIX

Table 3. Clinical classification of the New York Heart Association based on the past and present disability uninfluenced by physical signs

HELLO, HAPPY PILL!

Table 4.WHO risk classifIcation of CVD & pregnancy

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Table 5. Summary of Valvular Heart Diseases

Table 6. Comprehensive Clinical Classification of Pulmonary HTN

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