HEART DISEASE COMPLICATING PREGNANCY Moderator-Dr.Kushla pathania Presented byDr.

Pankaj Sharma

 Increase in plasma volume by 40 to 50 percent Increase in cardiac outputby 30 to 40 percent Increase in heart rate 10 to 15 BPM Decrease in blood pressure by 10 mmHg. Increase in red cell volume(15-20%) These changes are normal in pregnancy

Physiological Cardiovascular Changes in Pregnancy

ECG CHANGES IN NORMAL PREGNANCY

Shift in QRS axis to left or right Due to changes in position of heart non specific ST & T wave changes

Changes in the postpartum period

The blood volume decreases by 10% within the first 3 days hemoglobin level and the hematocrit increase progressively for the first 2 wks Within 2 weeks systemic vascular resistance increases by 30%

Cont.
After the initial tachycardia associated with labour a bradycardia often develops in the early puerperium. The heart rate slowly returns to baseline levels over the next 2 weeks. There is an immediate increase in cardiac output after delivery (within the first hour) by as much as 80%. After this there is a decrease over the next 4 weeks. ( GABBE 5th ed.)
5

The clinical features in a normal pregnancy which can mimic a cardiac disease are 1. Dyspnea - due to hyperventilation, elevated diaphragm. 2. Pedal Edema 3. Cardiac impulse- Diffused and shifted laterally from elevated diaphragm. 4. Jugular veins may be distended and JVP raised. 5. Systolic ejection murmurs along the left sternal border occur in 96% of pregnant women and are believed to be caused by increased flow across the aortic and pulmonary valves.

6 Continuous murmur at 2nd to 4th intercostal space-mammary souffle 7 Loud 1st heart sound with splitting 8 Loud 2nd heart sound 9 3rd & 4th heart sound in few cases 10 Anemia

Classification of heart disease in preg nancy

1. Rheumatic heart disease
Mitral Mitral Aortic Aortic stenosis (most common) regurgitation stenosis regurgitation

2. CONGENITAL HEART DISEASES

I NONCYNOTIC ASD VSD PULMONARY STENOSIS COARCTATION OF AORTA II CYANOTIC FALLOTS TETROLOGY EISSENMENGER SYNDROME 8

Miscellaneous
Mitral valve prolapse Cardiac arrythmias Peripartum cardiomyopathy Ischemic heart disease Marfan syndrome

Heart disease in pregnancy

The overall incidence of serious heart disease complicating pregnancy is approximately 1%. During the last few decades, the etiology of heart disease in developed countries has changed from primarily rheumatic to predominantly congenital

(JAMES HIGH RISK 4th ed)

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Incidence in India
According to a study carried out in an Indian medical institute, the incidence of heart disease in pregnncy was estimated to be 1.3%. This study indicated that rheumatic heart disease was the commonest heart condition (78%) of which mitral stenosis was the commonest heart defect (71.54%). Congenital heart disease (18.7%) is the second most common heart condition in pregnancy. (https://www.quest4health.com)
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NYHA Classification of Heart Disease

Class I. Uncompromisedno limitation of physical activity Class II. Slight limitation of physical activity Class III. Marked limitation of physical activity Class IV. Severely compromisedinability to perform any physical activity without discomfort 12 WILLIAMS 23rd ed)

Predictors of cardiac complications based on scoring system (2001) Prior heart failure, transient ischemic attack, arrhythmia, or stroke. Baseline NYHA class III or IV or cyanosis. Left-sided obstruction defined as mitral valve area less than 2 cm2, aortic valve area less than 1.5 cm2, or peak left ventricular outflow tract gradient above 30 mm Hg by echocardiography Ejection fraction less than 40 percent (Williams 23rd ed)
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Indicators of Heart Disease During Pregnancy

Symptoms Progressive dyspnea or orthopnea Nocturnal cough Hemoptysis Syncope Chest pain

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Clinical Findings
Cyanosis Clubbing of fingers Persistent neck vein distension pansystolic murmur grade 3/6 ,late systolic,louder ejection systolic Diastolic murmur Persistent split second heart sound.

( WILLIAMS 23rd ed.)

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INVESTIGATIONS
ECG:Arrhythmias,biatrial enlargment & 24-hour ECG monitor may be indicated if rhythm disorder suspected Chest x-ray:cardiomegaly,prominent vascular markings. ECHO:Structural abnormalities,Flow gradients etc. Cardiac MRI :Can delineate complex anatomy when not evaluated by echo

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complications of cardiac disease in pregnancy

Maternal effects:depends up on etiology,type of lesion,functional status,antenatal care and can be Congestive cardiac failure Bacterial endocarditis Pulmonary edema Acute rheumatic carditis Pulmonary embolism Rupture of aneurysm in coarctation of aorta Pre term labour Maternal death 17 Arrythmias

 Congestive cardiac failure occurs at 68wks,30-34 wks,2nd stage of labour,immediate post partum,5days post partum,5 months after delivery. Acute rheumatic carditis seen in 1st trimester Subacute bacterial endocarditis occurs In 1% & should be suspected if patient has fever,rapid hemodynamic deterioration,& leukocytosis without any source of infection
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 Chances of embolism more in immobilised patients & with prosthetic valves &cardiomyopathy

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Mortality associated
Low risk of maternal mortality (less than 1%). (a) Septal defects. (b) New York Heart Association classes I and II. (c) Patent ductus arteriosus. (d) Pulmonary / tricuspid lesions.

( DE SWIET 5th ed)

20

Mortality associatedCONT
Moderate risk of maternal mortality (515%). (a) NYHA classes III and IV mitral stenosis. (b) Aortic stenosis. (c) Marfans syndrome with normal aorta. (d) Uncomplicated coarctation of aorta. (e) Past history of myocardial infarction.
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REF.DE SWIET

High risk (Mortality 25-50%)

Pulomonary hypertension Eisenmenger syndrome Severe aortic stenosis Marfan syndrome with aortic root dilatation or major valvular involvement. COA with valvular involvement

22

Maternal prognosis
Pregnancy does not affect survival after pregnancy Prognosis becomes clear at 28-32 wks In subsequent pregnancy tendency to fall in lower functional class

23

Fetal effects
Miscarriage Prematurity Fetal growth restriction Increased congenital malformations(310%) Fetal death

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Fetal prognosis
In RHD prognosis good though perinatal mortality slighty more and birth wt on average 200gms less than for normal patients Chances of pre term in case of advance disease In case of congenital diseases poor prognosis & depends up on degree of cyanosis Chances of fetus being affected is 2-3% if father affected & 5-6% if mother affected
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General management principles

Aim is prevention,early diagnosis, appropriate treatment All women should be counselled before pregnancy. Women with contraindications advised not to conceive Those with valvular lesions should conceive when they are in NYHA class I&II Those with severe disease eg severe MS should undergo surgery before pregnancy
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Indications for MTP

ABSOLUTE Eisemengers syndrome Primary pulmonary hypertension Single ventricle marfans syndrome with aortic root diameter>7cm Peripartum cardiomyopathy Pulmonary veno occlusive disease

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Indications for MTP

Relative Severe obstructive lesion Parous women with NYHA III&IV History of cardiac failure

When to do? Termination should be done using S&E Before 12wks preferably 8wks

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Ante natal care

OBJECTIVE: To minimise factors that encroach up on limited circulatory reserve Should be seen regularly by cardiologist & Senior obstetrician Counsel about specific lesions ,functional cardiac status,complications ANC every 2wks till 30wks then every week Adequate rest Educate about symptoms of worsening of cardiac status Salt restriction General physical examination at each visit
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 Careful vigilance for preeclamsia Early diagnosis & treatment of UTI,RTI,dental infection. All women with RHD should receive Pencillin prophylaxis(benzathine pen.1.2 mega units)or erythromycin if patient allergic 250mg BD throughout pregnancy Fetal monitoring routine USG, fetal ECHO, NST,BPP.

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INDICATIONS FOR ADMISSION

Women with class III&IV should be admitted when diagnosed untill delivery or functional status improves Class I&II admitted 2wks prior to expected date of delivery Worsening of cardiac status Cardiac failure Appearnce of symptoms & sign like cough, dysnea,basal lung crepitations

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Management of labour and delivery

Generally vaginal delivery best induction best avoided unless obstetric indication Casearean for obstetric indication INDICATIONS FOR CESAREAN Obstetric indications Large aortic aneurysm

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 Semirecumbent position with lt. lateral tilt i/v fluids restricted to 75ml/hr except in AS Oxygen inhalation 5-6 l/min labour analgesia/ (morphine/epidural ) CVP monitoring in high risk patients Monitoring for CCF as follows: pulse>100/min RR>24 Dyspnea JVP Cyanosis 33 Basal crepitations

Management of first stage of labour

i/v

Prophylactic antibiotics

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 Invasive monitoring by PAC in high risk cases. SECOND STAGE MANAGEMENT Cutting short 2nd stage not in every case When required than by forceps or vaccum

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Third stage management

Oxytocin 10 units i.m. except in lt. to rt. Shunts or sever outflow obstruction Avoid methergin Misoprost can be given

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Management in puerperium
1st 12hrs crucial Bed rest in propped up position Sedatives Half hourly vitals monitoring Breast feeding except if patient in heart failure Watch for sign symptoms of CCF Treat infections if any

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contraception
Barrier methods POPs can be given DMPA good option IUCD relatively contraindicated Ocps contraindicated

Vasectomy of husband , mini laprotomy Laproscopic sterlisation not advisable

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Management of complications
CONGESTIVE CARDIAC FAILURE Bed rest Salt intake restriction Diuretics 40-80mg i/v frusemide f/b 40mg daily Serum potassium monitoring daily

39

Management of arrythmias
Digoxin drug of choice .25mg i/v every 2hrs up to maximum of 1.5mg & maintenance dose of .125-.25mg Diltiazem .25mg/kg i/v over 2min. Then 5-15mg/hr infusion or 120-360mg oral in divided doses. Cardioversion in chronic & hemodynamically unstable patients Anticogulation in chronic arrythmias Other drugs esmolol,metoprolol,propranol verapamil
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Management of acute pulmonary edema

Propped up position Oxygen inhalation Morphine 5mg i/v repeated 5-10 minutes up to maximum dose of 15mg. Diuresis with frusemide Monitorning of oxygen saturation

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Infective endocarditis
Admit patient Antibiotics Pencillin G 10-20 m units i.m/i.v and gentamicin 1.5mg/kg body weight 8hrly for 2wks vancomycin 15mg/kg i/v 12hrly 4wks watch for CCF & treat accordingly Maternal mortality 20-25%

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Surgical and percutaneous interventions in pregnancy

CLOSED MITRAL VALVOTOMY Can be carried out at any stage Indications Failure of medical therapy with intractable symptoms Profuse haemoptysis History of pulmonary edema before pregnancy ProvidedNo calcification of valve No associated MR
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Balloon valvuloplasty
It has replaced valvotomy Prerequisits areNon calcified valve No major MR Done between 24-28wks COMPLICATIONSAcute MR Procedural tamponade Thromboembolism Only <2%

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Mitral valve replacement

Although usually postponed until after delivery, valve replacement during pregnancy may be lifesaving in case of life threatening pulmonary edema. Maternal mortality 1-5% Fetal mortality 20-33% it is recommended that surgery is done electively pump flow rate is maintained 2.5 L/min/m2, normothermic perfusion pressure is 70 mm Hg, hematocrit is 28 percent. 45

Choice of valve
Porcine tissue valves are much safer during pregnancy, primarily because anticoagulation is not required as thrombosis is rare . To the contrary, valvular dysfunction, deterioration,or failure are common, and develop in 5 to 25 percent Another drawback is that bioprostheses are not as durable as mechanical ones, and valve replacement averages every 10 to 15 years.
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CORRECTION OF CONGENITAL DEFECTS

INDICATIONS Fast worsening symptoms Class IV status in early pregnancy History of deterioration in previous pregnancy

Best time- 20-24 wks if any choice

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Pregnancy in women with prosthetic valves

Mechanical valves and anticoagulation were associated with a moderate increase in miscarriage and thromboembolic events. Mechanical valves were associated with a maternal mortality rate of 3.7 percent and a thromboembolic rate of 14.8 percent. Thromboembolism was increased fourfold with heparin use rather than warfarin. Mitral valves accounted for 81 percent of thrombotic complications.

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American College of Chest Physicians Guidelines for Anticoagulation of Pregnant Women with Mechanical Prosthetic Valves Adjusted-dose LMWH twice daily throughout pregnancy. manufacturers peak anti-Xa level 4 hours after subcutaneous injection. Adjusted-dose UFH administered every 12 hours

The doses should be adjusted to achieve the

an anti-Xa heparin level of 0.35 to 0.70 U/mL. LMWH or UFH as above until 13 weeks gestation with warfarin substitution until close to delivery when LMWH or UFH is resumed

throughout pregnancy. The doses should be adjusted to keep the midinterval aPTT at least twice control or attain

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INDIVIDUAL LESIONS

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1. mitral stenosis
Rheumatic endocarditis causes three fourths of mitral stenosis cases. In a 12-year review of 486 pregnant patients in India through 1999, 63% of lesions affected a single valve. Mitral stenosis was the abnormality in 90% of these women

(JAMES 4th ed)

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CONT.
The normal mitral valve surface area is 4 -6 cm2. When less than 2.5 cm2,symptoms usually develop. Rheumatic fever results in: Leaflet thickening, Commissural fusion Retraction of the chordae tendineae

de swiet 5th ed

52

MS CONT.
Those native to a developed country, usually does not present until after age 30. Rapidly progressive in the natives of developing world so one should have a higher index of suspicion Mitral stenosis restricts left ventricular inflow, with resultant elevation of the left atrial and pulmonary venous pressures. DE SWIET 5th ed

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MS CONT.
The diagnosis is made on echocardiography and classified as follows:mild 1.52.0 cm2 moderate 11.5 cm2 severe <1.0 cm2.

de swiet 5th ed
54

Cardiac examination: may reveal a loud S1 (S1 is as loud or louder than S2 when listening over the aortic or pulmonary area) opening snap (a sound heard shortly afterS2) a diastolic rumbling murmur signs of right ventricular strain and pulmonary hypertension may become apparent de swiet 5th ed
55

Ms cont.
Patients with mild-to-moderate or occult mitral stenosis may first become symptomatic during pregnancy. Increased volume and heart rate adversely affect cardiovascular hemodyanmics in rheumatic mitral stenosis clinical deterioration during gestation should be expected.

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MS CONT.
The flow of blood from the left atrium to the left ventricle during diastole is limited. The normal mitral valve area is 4.0 to 5.0 cm2. Symptoms with exercise can be expected with valve areas less than or equal to 2.5 cm2. Symptoms at rest are expected at less than or equal to 1.5 cm2. GABBE 5th ed

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MS CONT.
The left ventricle responds with Starling mechanisms to increased venous return with increased performance, elevating CO in response to demand. The left atrium is limited in its capacity to respond. Therefore, CO is limited by the relatively passive flow of blood through the valve during diastole. Increased venous return results in pulmonary congestion rather than 58 increased CO.

MS CONT
The relative tachycardia experienced in pregnancy shortens diastole, decreases left ventricular filling, and therefore, further compromises CO and increases pulmonary congestion.

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DIAGNOSIS
Diagnosis in pregnancy before maternal decompensation is uncommon. Tiredness and dyspnea on exertion are characteristic symptoms of mitral stenosis. Hemodynamic tolerance is generally good during the first trimester because tachycardia and increase in cardiac output are still moderate. Symptoms generally begin during the second trimester

Celia Oakley

2nd

ed.

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DIAGNOSIS CONT
Theoretically, clinical diagnosis should be easier during pregnancy because the intensity of the murmur tends to increase with cardiac output. but perception of the murmur may be difficult because of tachycardia Intercurrent event such as a febrile episode will result in exaggerated symptoms Under these circumstances, echocardiogram should be performed to rule out mitral valvular disease.
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Diagnosis
Echocardiographic diagnosis of mitral stenosis is based on the characteristic appearance of stenotic,frequently calcified valve Calculation of valve area from pressure half-time of the Doppler wave or by two-dimensional planimetry provides an objective measure of severity. Gabbe 5th ed
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MANGEMENT OF MS

PREPREGNANCY ANTE NATAL INTRAPARTUM POSTNATAL

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 The goal of preconception care is to define the severity of cardiac compromise Two-dimensional echocardiography and color-flow Doppler are used to determine cardiac function and the degree of stenosis In symptomatic patients or those with severely stenotic valves, surgical correction should be done before conception Surgical commissurotomy/Percutaneous mitral valve commissurotomy james 4th ed 64

PRE PREGNANCY

ANTEPARTUM
The goal of antepartum care is to achieve a balance between the drive to increase CO and the limitations of flow across the stenotic valve. Limited physical activity If symptoms of pulmonary congestion develop:activity is further reduced, Dietary sodium is restricted Diuretic therapy is started B-blockers usually given to blunt the cardiac response to activity and anxiety
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CONT.
If new-onset atrial fibrillation develops,intravenous verapamil, 5 to 10 mg, is given, or electrocardioversionis performed. For chronic fibrillation, digoxin, B blocker,or a calcium-channel blocker is given to slow ventricular response. Therapeutic anticoagulation with heparin is indicated with persistent fibrillation

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CONT.
Serial echocardiography is indicated to follow cardiac function. Percutaneous mitral balloon valvulotomy may be necessary to treat patients with significant functional deterioration or refractory pulmonary edema, despite optimal medical management. Women with a history of Rheumatic valvular disease should receive prophylaxis with daily oral penicillin G or monthly benzathine penicillin. WILLIAMS 23rd ,GABBE 5th, JAMES 4th ed

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INTRAPARTUM
During the intrapartum period, volume status and cardiac output are critical concerns In patients with NYHA class III or IV disease, central hemodynamic monitoring pulmonary Capillary wedge pressure (PCWP) can warn of the potential for pulmonary edema, Fluid restriction or careful diuresis, with attention to cardiac output, may be used to obtain desirable pressures 68

 Careful intravenous administration of -blockers Epidural analgesia is both safe and effective. Cesarean delivery is typically reserved for obstetric indications Although forceps delivery is advocated to shorten the second stage of labor and reduce bearing down, it is not always required Endocarditis antibiotic prophylaxis should be given prior to cesarean section 69 .JAMES 4th ed

CONT

POSTNATAL
Postpartum fluid shifts increase the risk of pulmonary edema. PCWP increase by 10 mm Hg between the second stage of labor and the postpartum Because frank pulmonary edema is unlikely at a PCWP of less than 30 mm Hg, maintaining the PCWP at 14 mm Hg or lower if central hemodynamic monitoring is employed should prevent this complication JAMES 4th ed
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PREGNANCY OUTCOMES
complications are directly associated with the degree of valvular stenosis Canadian study found that women with a mitral-valve area 2 cm2 were at greatest risk for complications. In another study from California on 46 pregnant women with mitral stenosis, Complications included heart failure in 43 percent and arrhythmias in 20 percent. williams 23rd ed
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Cont.
Fetal-growth restriction was more common in those women with a mitral valve area less than 1.0 cm2 Among 486 pregnancies complicated by rheumatic heart disease predominantly mitral stenosisSawhney and associates reported that eight of 10 maternal deaths were in women in NYHA classes III or IV. williams 23rd ed
72

Aortic stenosis
Aortic stenosis is the most common cardiac valve lesion in the United States. It can be : congenital rheumatic age-related calcification of the aortic valve All of these causes are uncommon in women of reproductive age Although congenital aortic stenosis is the most frequent etiology seen during pregnancy. 73 th ed JAMES 4

CON
Aortic stenosis of rheumatic origin is typically progressive Tends to be less severe in patients of reproductive age. It accounts for only 5% to 10% of cases of rheumatic heart disease in pregnancy Usually seen in conjunction with mitral valve disease.
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CONT.
The normal aortic valve area is 3 to 4 cm2. The pressure gradient across the valve increases rapidly as the valve area is reduced to less than 2 cm2. This increase is associated with left ventricular outflow obstruction Mild to moderate congenital stenosis (valve area > 1 cm2) is relatively well tolerated in pregnancy, and cardiac complications typically do not occur
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DIAGNOSIS
Young women with aortic stenosis are usually asymptomatic. Although they may develop increasing exercise intolerance in pregnancy, the progression is insidious and not easily distinguished from the effects of normal pregnancy. The diagnosis is usually made by the auscultation of a harsh systolic murmur. Diagnos is confirmed by echo

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HEMODYNAMICS
Aortic stenosis is a condition of excess left ventricular afterload. Ventricular hypertrophy increases cardiac oxygen requirement. whereas increased diastolic ventricular pressure impairs diastolic coronary perfusion. Each increases the potential for myocardial ischemia.

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Cont.
The left ventricle requires adequate filling to generate sufficient systolic pressure to produce flow across the stenotic valve. Given a hypertrophied ventricle and some degree of diastolic dysfunction, the volume-pressure relationship is very steep A small loss of left ventricular filling results in a proportionately large fall in left ventricular pressure and, therefore, a large fall in CO.
78

Cont.
The pregnant patient with significant aortic stenosis is very sensitive to loss of preload associated with hemorrhage or epidural induced hypotension.

The window of appropriate filling pressure is narrow Excess fluid may result in pulmonary edema & insufficient fluid may result in hypotension and coronary ischemia
79

Cont.
In general, pulmonary edema associated with excess preload is much easier to manage than hypotension due to hypovolemia.

80

MANGEMENT
PRE PREGNANCY The severity of aortic stenosis should be determined by echocardiography. Severe disease should be corrected surgically before conception.

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ANTENATAL
Physical activity should be limited. Patients should be observed for signs of congestive heart failure or arrhythmias. Serial fetal ultrasounds should be scheduled to detect evidence of growth restriction Given that most aortic stenosis in young women is congenital in origin, fetal echocardiography is indicated.

82

ANTENATAL
Hospital admission one day before planned induction of labor with a favorable cervix is preferred. A prolonged induction should be avoided. The patient should be gently hydrated overnight to achieve a pulmonary artery wedge pressure (PAWP) of 12 to 15 mm Hg An elevated PAWP serves as a buffer against a loss of preload.
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INTRAPARTUM
Fluid management is the critical component of intrapartum care. hypotension is of more concern. Patients should labor and deliver in the lateral position. Regional anesthesia is administered slowly and cautiously, after adequate volume loading. Use of a PAC may aid in monitoring volume status in Patients with gradients above 60 to 80 mm Hg JAMES 4th & GABBE 5th ed 84

Cont.
A narcotic epidural can decrease the occurrence of hypotension. Pulmonary edema no overaggressive diuresis Oxygen supplementation. morphine Dopamine or dobutamine ,maintain cardiac output. Bacterial endocarditis prophylaxis is recommended for cesarean delivery. JAMES 4th ed
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POSTNATAL
Postpartum, patients should be monitored hemodynamically for 24 to 48 hours. Diuresis is usually spontaneous the patient can be allowed to find her predelivery compensated state. When diuresis must be induced to treat pulmonary edema, it should be done gently and carefully. Predelivery hemodynamic parameters should be used as an endpoint GABBE 5th ed
86

Coarctation of the Aorta

Coarctation of the aorta results from a constriction of the aorta at or about the level of the ductus arteriosus or left subclavian artery.

Patients have a characteristic discrepancy in blood pressure between their right arm and lower extremities
Untreated coarctation of the aorta carries a poor prognosis and is uncommon today.

87

 Several cardiovascular anomalies are associated with coarctation of the aorta. A bicuspid aortic valve is the most common, found in (85%) of patients. VSDs, anomalies of the intercostal and subclavian arteries, and aneurysms of the circle of Willis(69%) may also be present. Hypertensive disorders of pregnancy arecommon and reported in more than 15% of patients. JAMES 4th DE SWIET 5th ed
88

CONT.

CONT.
A systolic or occasionally continuous murmur can be heard in the infraclavicular or scapular area Some patients will only present later in life with hypertension Delay between brachial and femoral pulses

89

CONT
Although data are limited, the physiologic changes associated with pregnancy may unmask and aggravate postrepair gradients. Aortic rupture or dissection is rare True claudication is rare due to collateral circulation.

90

RISK IN PREGNANCY
Include worsening hypertension New-onset heart failure Rarely but ominously, aortic dissection and rupture

91

 Termination may be considered in patients with uncorrected coarctation of the aorta The majority of patients will have had a previous repair and require evaluation The highest risk of rupture or dissection is in patients with a Dacron patch repair Fetal echocardiogram. Ideally, moderate-to-severe aortic coarctation should be repaired, with balloon angioplasty or stenting, or replacement prior to pregnancy
92

Mangement

 Maternal management includes: limitation of physical activity Maintenance of systolic blood pressure close to 140mmHg Beta-blockers are the agent of choice Vaginal delivery,with an assisted second stage to reduce Valsalva, is preferred. Increased hypertension and myocardial oxygen demand can be reduced by the use of beta-blockers Adequate pain control, particularly with the use of epidural anesthetics.
93

CONT.

Pulmonary Stenosis
Pulmonary valve stenosis is the most common type of isolated right ventricular outflow tract obstruction. Almost always congenital in origin. Associated with a systolic ejection murmur at the left upper sternal border and often a fixed split S2. Severe stenosis is usually associated with right-sided heart failure Repaired with surgical or balloon valvotomy in childhood
94

Cont..
congenital pulmonary valve stenosis should have percutaneous balloon valvuloplasty before conception. These patients are often left with some degree of insufficiency,but tolerated well. Patients with unrepaired mild-tomoderate pulmonary stenosis(gradients < 40 mmHg) usually asymptomatic and tolerate the hemodynamic burden of pregnancy
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Atrial septal defects

The most common congenital lesions in adults may be first diagnosed during pregnancy. There are three types The most common 80%, is the secundum type. The secundum ASD(located in the central portion of the atrial septum) is associated with myxomatous mitral valve disease and prolapse in 2030% of cases. 96

CONT.
The more unusual types are: Primum, or endoardial cushion, defects ( in the lower portion of the atrial septum), which are most commonly associated with Downs syndrome Sinus venosus defects (located in the upper portion of the atrial septum) in which the right upper pulmonary vein is usually emptying into the superior vena cava and right atrium.
97

 The uncorrected left-to-right shunt produces a volume load on the right side with enlargement of the right atrium and ventricle. The flow across an ASD is not very turbulent and runs down a low gradient Does not directly cause an audible murmur; however, increased flow across the pulmonary valve may cause a 2/6 systolic ejection flow murmur. ASD causes a wide fixed split second heart sound with the patient in the sitting/standing position
98

 Signs of right ventricular hypertrophy and pulmonary hypertension can be present in advanced and severe cases. ASD are typically asymptomatic but may be associated with: atrial arrhythmias, stroke from paradoxic emboli, migraine right heart failure.

99

DIAGNOSIS
The diagnosis can usually be made on transthoracic echocardiography but may need transesophagealechocardiography to detect some smaller shunts and sinus venosus defects.

100

Hemodynamics &Pregnancy outcome

The expected 50% increase in blood volume during pregnancy causes further volume loading, Most patients with an isolated ASD tolerate pregnancy well ventricular ejection fraction and NYHA functional status are predictive of uncomplicated and successful outcomes

101

 With larger defects and shunts, there is risk for congestive heart failure, atrial arrhythmias, peripheral venous thrombosis or embolism, cerebral vascular accidents, and shunt reversal Congestive heart failure can be treated medically with digoxin and diuretics. Atrial arrhythmias can worsen or precipitate heart failure and should be treated with beta-blockers and digoxin.
102

low-dose aspirin after the first trimester is advocated to reduce the risk of venous thrombosis and hence paradoxic emboli. Systemic hypotension, which can occur during parturition and epidural anesthesia, should be anticipated and corrected to prevent possible shunt reversal and oxygen desaturation. Preconception closure of the defect is recommended for women with symptoms, arrhythmias or significant right-to-left 103 shunts where ( Qp / Qs ) is 1.5:1

VSD
Ventricular septal defects (VSD) are common at birth (0.33 /1000 livebirths) but Many close spontaneously in childhood The size and location of the defect affect the clinical course. The most common type of defect occurs in the membranous septum or left ventricular outflow tract

104

 The flow across a VSD produces a loud (typically 46/6) systolic ejection murmur Clinical sequelae and symptoms are most likely to happen if the VSD is large Effects of chronic volume overload and secondary pulmonary hypertension begin to manifest as exercise intolerance, dyspnea or congestive heart failure.

105

 Infective endocarditis, however, can occur with any size of VSD. Similarly to ASD, VSD should be repaired if symptomatic or associated with an elevation in pulmonary artery pressure. Isolated VSD are usually well tolerated in pregnancy unless the size is large

106

Peripartum risks are determined by:Left ventricular size and function, Pulmonary artery pressures, Functional class . In hemodynamically significant shunts, complications include:congestive heart failure, atrial arrhythmias pulmonary artery hypertension, shunt reversal. In women with corrected lesions, no increased risks
107

Patent ductus arteriosus

Patent ductus arteriosus is the persistence after birth of the direct connection between the pulmonary and arterial circulation Incidence of Isolated, persistent patent ductus arteriosus 1:2000 newborns, but rarely in adults. The residual embryonic shunt is from the descending aorta at the isthmus to the proximal left pulmonary artery

108

 Clinical symptoms and complications are also similar to those associated with VSD. Physical examination classically reveals a grade 46/6 continuous(diastolic and systolic), machinery murmur that is best heard at the upper left sternal border or infraclavicular area. Risks of pregnancy are related to shunt size and degree of pulmonary hypertension
109

In small shunts, maternal and fetal outcomes are not altered Theoretical risk of shunt reversal Patients with large shunts have enlargement of the pulmonary artery and left-sided chambers and can develop high-output heart failure. In corrected or uncorrected patent ductus arteriosus, pulmonary hypertension significantly increases maternal and fetal morbidity and mortality rates
110

MITRAL REGURGITATION
Mitral regurgitation may be due to a chronic progressive process such as rheumatic valve disease or myxomatous degeneration of valve Frequently associated with mitral valve prolapse. As regurgitation increases over time, forward fl ow is maintained at the expense of left ventricular dilation with eventual impaired contractility.

111

HEMODYNAMICS
The hemodynamic changes associated with pregnancy can be expected to have mixed effects. A reduction in SVRtends to promote forward flow. The drive to increase CO will exacerbate left ventricular volume overload. Increased atrial dilation may initiate atrial fibrillation Pulmonary congestion
112

Preconceptional counseling
valve replacement in consultation with a cardiologist. In general valve replacement is recommended for: symptomatic patients atrial fibrillation ejection fraction less than 50 to 60 percent left ventricular end-diastolic dimension greater than 45 to 50 mm, or pulmonary systolic pressure greater than 50 to 60 mm Hg.
113

Labour & Delivery

standard cardiac care. Catecholamine release due to pain or stress impairs forward flow. Particular attention should be paid to left ventricular filling. Excessive preload results in pulmonary congestion. Insufficient preload will not fill the enlarged left ventricle and will result in insufficient forward flow
114

Manag.
A pulmonary artery catheter can be used to determine appropriate filling pressure in early labor or before induction. The pulmonary artery diastolic pressure can be used as a reference point. Diuresis in the early postpartum period may be required. Acute mitral regurgitation uncommon and may be associated with ruptured chordae tendineae due to endocarditis or myxomatous valve disease. 115

Manag..
Without time for left ventricular compensation, forward flow may be severely compromised. Urgent valve surgery is usually required. Inotropic left ventricular support and systemic after load reduction can be used to stabilize the patient.

116

AORTIC REGURGITATION
Aortic regurgitation is most often due to: A congenitally abnormal valve Marfans syndrome Endocarditis Rheumatic disease The reduction in vascular resistance associated with pregnancy tends to improve cardiac performance

117

MANAG..
Valve replacement is generally recommended for: (1) (NYHA) functional class III and class IV symptoms (2) an ejection fraction less than 50 percent (3) left ventricular end-systolic dimension greater than 55 mm

118

 Labor and delivery is managed with standard cardiac care. Pulmonary artery catheterization is not usually required. As the hemodynamic changes associated with pregnancy resolve, a rise in vascular resistance should be anticipated and after load reduction maintained.

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Ebsteins anomaly
Uncommon congenital heart lesion, a malformed tricuspid valve is apically displaced to a variable extent with:Tricuspid regurgitation Atrial dilation Limited right ventricular function Severe cases present in infancy, but many cases will first present in teenager or adults. Complications include CHF, arrhythmias, and paradoxic embolism
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Associated abnormalities are frequent Include ASD (50%) and Wolff ParkinsonWhite (WPW) syndrome (30%) Most patients can be treated medically More severe forms may develop right heart failure and require surgical correction

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 Preconception repair is preferable, particularly for patients with an interatrial communication Risk of congenital heart disease in the offspring remains high at 6% The maternal risks of pregnancy are low correspond with : Degree of tricuspid regurgitation Right ventricular function Presence of cyanosis DE SWIET 5th ed
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 Complications include CHF, arrhythmias, and paradoxic embolism Atrial arrhythmias may occur In the presence Wolf-Parkinson White (WPW)syndrome, atrioventricular conduction can become exceedingly rapid with resultant hemodynamic collapse

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 The most common cyanotic congenital heart defect found in children, adults, and pregnant women It occurs in 3.9 per 10,000 births and accounts for up to 10% of congenital heart disease. The four diagnostic abnormalities are VSD Deviation of the aorta to the right so that it over-rides the VSD, Infundibular pulmonic stenosis Secondary right ventricular hypertrophy de swiet 5th
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Tetralogy of Fallot

 Preconception repair is preferred Repair usually involves relief of the right ventricular outflow obstruction & closure of the VSD. corrected patients should have a preconception functional assessment to further define risk. Patients with corrected lesions, good residual right ventricular function and good functional status usually tolerate the increased hemodynamic stress of pregnancy. Prophylaxis with aspirin to reduce the risk of thrombosis and paradoxic emboli may be indicated 125

 Prophylaxis with aspirin to reduce the risk of thrombosis and paradoxic emboli may be indicated Uncorrected lesions can be expected to have clinical deterioration during pregnancy, resulting in increased maternal and fetal complications

de swiet 5th ed
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TRANSPOSITION OF THE GREAT VESSELS Transposition of the great vessels (TGV) is present in only 5 percent of pregnant women with congenital heart disease In complete TGV the aorta arises from the right ventricle and the pulmonary artery arises from the left ventricle venous blood returns to the right atrium, and passes through the tricuspid valve, into the RV, and directly into the transposed aorta

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 TGV was first definitively corrected in 1964 with the Mustard operationa Off late direct surgical switch between the pulmonary artery and the aorta has been performed. The hemodynamic changes of pregnancy will have a mixed impact on a patient with a Mustard repair.Increased CO increases the volume load on the right heart. and decreased vascular resistance reduces afterload on the right side of the heart
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 In surgically corrected patients complications that should be anticipated include : CHF due to limited cardiac reserve, Tachyarrhythmias Paradoxic emboli The fetal prognosis remains poor, with mortality close to 50% and prematurity and intrauterine growth restriction ranging from 30% to 50% GABBE 5th & DE SWIET 5th
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 Evaluation before pregnancy should include: Assessment of functional status Evaluation of heart function Confirmation of normal oxygenation. When the right side of the heart is the systemic heart, pharmacologic afterload reduction should be maintained until pregnancy is confirmed. Young women with surgically corrected TGV can be expected to successfully complete pregnancy GABBE 5th ed
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Eisenmengers syndrome
Severe pulmonary vascular obstructive disease and hypertension resulting from septal communication between the systemic and pulmonary circulations is termed Eisenmengers syndrome. Eventually the normally lower pressure right ventricle and pulmonary circulation begin to see pressures that approach the pressures on the normally higher pressure left heart.

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 Eisenmengers syndrome refers to the endstage of this process when equalization of pressures in the right and left heart causes the previous shunting to reverse so that unoxygenated blood that was intended for the pulmonary circulation enters the systemic circulation The hemodynamic changes of pregnancy and parturition are poorly tolerated in Eisenmengers syndrome .The maternal mortality rate may be as high as 39 52%; thus, pregnancy is contraindicated 132 de swiet 5th ed

Pulmonary hypertension
Although pulmonary hypertension is fundamentally a pulmonary disease, the major pathologic impact is on the right side of the heart. The incidence of primary pulmonary hypertension is 1 to 2 per 1 million, with women affected more commonly than men. The reported mortality of PH has ranged from nearly 60% in early reports, to as low as 25% more recently.
( Clin Chest Med 32 (2011) 165174&Gabbe)
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 Secondary pulmonary hypertension may develop as a complication of cardiac disease such as mitral stenosis or secondary to intrinsic pulmonary disease. Drugs such as cocaine or appetite suppressants may also be associated with pulmonary hypertension. The maternal mortality with severe pulmonary hypertension is reported to be as high as 50 percent. Sudden, irreversible deterioration in the postpartum period is common. 134 th ed Gabbe 5

Physiology
patients with preexisting PAH are unable to make adjustment to pregnancy induced cvs changes. The right ventricle, which now faces increased afterload from higher PVR, cannot accommodate the increase in cardiac output and becomes overloaded. This can result in progressive right ventricular failure and sudden death from arrhythmia.

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 The pain of parturition is associated with stimulation of the sympathetic nervous system and dramatic increases in heart rate, blood pressure, and myocardial oxygen consumption,and can be associated with vagal responses that can lead to hypotension and sudden death.

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CLASSIFICATION OF PH
According to the latest World Health Organization criteria, PAH is defined by a mean pulmonary artery (PA) pressure greater than 25 mm Hg at rest, A normal PA occlusion pressure (15 mm Hg), and increased PVR. REF.

.Clin Chest Med 32 (2011) 165174

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Updated clinical classification of pulmonary hypertension (Dana Point) Class 1: Pulmonary Arterial Hypertension Idiopathic Class 2: Pulmonary Hypertension Caused by Left side Heart Disease Class 3: Pulmonary Hypertension Caused by Lung Disease and/or Hypoxia Class 4: Chronic Thromboembolic Pulmonary Hypertension (CTEPH) Class 5: Pulmonary Hypertension with Unclear Multifactorial Mechanisms Clin Chest Med 32 (2011) 165174
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DIAGNOSIS AND SCREENING

The symptoms of pulmonary hypertension are nonspecific. Increasing fatigue and shortness of breath are associated with progressive right-sided heart failure The availability and improved technique of transthoracic echocardiography (TTE) has led to its widespread use as a screening tool for PH. Diagnosis of PAH during pregnancy must be confirmed by RHC
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PREGNANCY OUTCOMES AND MORTALITY &MANAGMENT

Poorly tolerated in pregnancy. A mortality rate approaching 50 percent should be expected. Antepartum management often requires hospitalization. Oxygen therapy may reduce pulmonary vascular resistance and improve right ventricular performance. Pharmacologic treatment with nifedipine or intravenous prostacyclin may also be effective.
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 Anticoagulation with heparin should be considered. Worsening disease will usually be manifest by falling CO rather than rising right ventricular pressure. Labor and delivery should be managed with standard cardiac care, with particular attention to right ventricular filling as assessed by measurement of central venous pressure (CVP)
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 Women with pulmonary hypertension and right ventricular dysfunction should be strongly discouraged from becoming pregnant.

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Peripartum cardiomyopathy
Peripartum cardiomyopathy is a rare syndrome Although rare, cardiomyopathy in pregnancy accounts for a significant proportion of maternal deaths Mortalities have ranged as high as18% to 56%

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INCIDENCE
The incidence with rates ranging from approximately 1:15,000 pregnancies in the United States to as frequent as 1:299 in a well-studied population in Haiti and 1:100 in a small region of subSaharan Africa.

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Diagnostic Criteria for Peripartum Cardiomyopathy

1. Heart failure within the last month of pregnancy or 5 months postpartum 2. Absence of prior heart disease 3. No determinable cause 4. Echocardiographic indication of left ventricular dysfunction: Ejection fraction <45 percent or fractional shortening <30 percent Left ventricular end-diastolic dimension >2.7 cm/m2 GABBE 5th edition
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Risk factors include: Hypertension Preeclampsia Multiparity Multiple gestations African descent older maternal age

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PATHOGENIC MECHANISMS
Investigation of the pathophysiology has been limited by the rare incidence For many years it was believed that PPCM was a variant of IDCM PPCM is its own distinct entity

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PATHOPHYSIOLOGY

Int J Cardiol 2009;131:16879;

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Recommended therapy for PPCM

Goals Treat hypertension Fluid restriction Dietary salt restriction Routine exercise post partum if stable Drugs for routine use Diuretics b-Blockers Vasodilators Digoxin

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Therapies in selected patients

Inotropes Anticoagulation Implantable defibrillators Biventricular pacing Cardiac transplantation

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 Serial clinical assessment should be performed at each return visit assessment of ejection fraction and structural heart changes should be performed in patients who have had a change in clinical status Serial measurements of BNP to guide therapy Serum electrolytes and renal function should be monitored frequently
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 A sonogram at 20 weeks gestation to assess fetal anatomy, then serially to assess fetal growth Antenatal testing (nonstress test and biophysical profile) starting at 32 weeks and then weekly thereafter Fett recently proposed a focused medical history test for PPCM patients during the latter portion of the pregnancy and post partum period.
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Evaluating for: orthopnea, dyspnea, unexplained cough, lower extremity swelling, excessive weight gain Palpitations Tests for natriuretic peptide levels and high-sensitivity CRP (hs-CRP) are performed if the patient has 3to 4 points or more, with repeat echocardiography if these are increased
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MANAGEMENT OF DELIVERY
If medical management is successful in stabilizing a patient with PPCM, then early delivery is not required and spontaneous labor is not contraindicated Labor induction can be conducted with minimal risk and, if cervical ripening is required: prostaglandins oxytocin Avoid fluid overload Shortening the second stage of labor with the use of low forceps or a vacuum device is recommended to minimize ventricular work
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 Cesarean delivery for obstetric indications We reserve invasive monitoring for individuals in whom volume status is problematic. Thromboprophylaxis Strict monitoring of fluid status Diuretic therapy after delivery The parturient should be seen 1 week after delivery to assess her cardiovascular status
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MARFANS SYNDROME
an autosomal dominant genetic disorder caused by an abnormal gene for fibrillin chromosome 15. Disease prevalence is estimated to be four to six per 10,000. abnormal connective tissue results in the characteristic feature of the disease: aortic root dilation, dislocation of the optic lens, deformity of the anterior thorax, scoliosis, long limbs, joint laxity, and arachnodactyly.
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 Diagnosis is usually based on family history, and physical examination, including ocular, cardiovascular, and skeletal features. Untreated, life expectancy is reduced by a third, with the majority of deaths due to aortic dissection and rupture. elective repair has been recommended when the aortic root diameter measures 5.5 to 6.0 cm.

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 The predicted diameter for young adults can be calculated: ADpredicted = 1.02 + (0.98 .body surface area [BSA]). A ratio of less than 1.3 with a dilation rate of less than 5 percent/y suggests a low risk for a cardiovascular event. Maternal mortality rate associated with Marfans syndrome in pregnancy in excess of 50 percent studies suggest that women with mild disease, an AD less than 4.0 cm
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 Women with ADs greater than 5.5 cm should certainly be counseled to have graft and valve replacement before pregnancy

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Management of pregnancies affected by Marfans syndrome

An accurate assessment of the aortic root. The aortic root should be protected from hemodynamic forces with blockade. A resting HR of approximately 70 beats per minute to be achieved Labor and delivery is managed with standard cardiac care, with particular emphasis on the prevention of tachycardia. Patients with aortic roots less than 4.0 cm can be delivered vaginally, reserving cesarean delivery for obstetric indications.
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Coronary Artery Disease

Acute myocardial infarction (AMI) during pregnancy is rare 1 in 35,000 pregnancies. Independent predictors of AMI during pregnancy include chronic hypertension, maternal age, diabetes, and preeclampsia. Most myocardial infarctions occur during the third trimester in women older than 33 year & multiparous

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 Maternal mortality is highest in the antepartum and intrapartum periods. 5% to 7% case-fatality rate in women with pregnancy-associated AMI Therapy modified in the pregnancy Thrombolytic agents increase the risk of maternal hemorrhage substantially (8%) Used in situations in which cardiac catheterization facilities are not available
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 Low-dose aspirin and nitrates are considered safe. Beta blockers are generally safe. Short-term heparin Clopidogrel and glycoprotein IIb/IIIa receptor inhibitors safe Percutaneous coronary intervention using both balloon angioplasty and stenting can be performed

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Anesthetic concerns for pregnant women with cardiac disease

Regional analgesia & anasthesia except most severe disease Manipulate timing of anticoagulant drugs to allow a window and minimize concerns about spinal hematoma Slow, cautious, incremental onset of regional block is essential

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 Important points to consider with epidural analgesia in labor include the following: Bupivacaine 0.1% with fentanyl 24 g/mL. Minimize aortocaval. Inject local anesthesia in a slow, incremental fashion.

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Anesthesia for cesarean section

There is no evidence available to support either regional or general anesthesia as being the safer. Each case must be assessed individually. There is a growing trend towards the slow, careful induction of regional block The advantages of regional anesthesia for CS are as follows: Avoid the catecholamine rise associated with endotracheal intubation and extubation. Neonate less likely to require ventilatory support
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General anesthesia for CS

Involve a cardiac anesthesiologist Antacid prophylaxis Intraoperative transesophageal echocardiography (TEE). Arterial line usually helpful. Position mother with a 15 lateral tilt. Use GA technique that will minimize cardiovascular changes.

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The disadvantages of GA for CS

Risk of aspiration of gastric contents. 1 in 300 risk of failed intubation. Hypertension and tachycardia on intubation. Reduction in venous return with mechanical ventilation. Negative inotropic effect of inhalational anesthetic agents. Neonatal sedation
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THANK YOU

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