heart disease complicating pregnancy

7/31/2019 Heart Disease Complicating Pregnancy

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HEART DISEASECOMPLICATING

PREGNANCYModerator-Dr.Kushla pathania

Presented by-

Dr. Pankaj Sharma

1



Physiological CardiovascularChanges in Pregnancy

• Increase in plasma volume by 40 to 50percent

• Increase in cardiac outputby 30 to 40percent

• 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

2



ECG CHANGES IN NORMALPREGNANCY

Shift in QRS axis to left or right

Due to changes in position of heart

non specific ST & T wave changes

3



Changes in the postpartumperiod

• The blood volume decreases by 10%within the first 3 days

• hemoglobin level and the hematocritincrease progressively for the first 2wks

• Within 2 weeks systemic vascularresistance increases by 30%

4



Cont.

• After the initial tachycardia associatedwith labour a bradycardia oftendevelops in the early puerperium. Theheart rate slowly returns to baseline

levels over the next 2 weeks.

• There is an immediate increase incardiac output after delivery (within the

first hour) by as much as 80%. Afterthis there is a decrease over the next 4weeks.

( GABBE 5th ed.)5



The clinical features in a normal pregnancywhich can mimic a cardiac disease are

• 1.

Dyspnea - due to hyperventilation, elevateddiaphragm.

• 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 sternalborder occur in 96% of pregnant women and are

believed to be caused by increased flow across theaortic and pulmonary valves.

6



6 Continuous murmur at 2nd to 4th intercostal space-mammary souffle

7 Loud 1st heart sound with splitting

8 Loud 2nd

heart sound9 3rd & 4th heart sound in few cases

10 Anemia

7



Classification of heart diseasein preg nancy

1. Rheumatic heart diseaseMitral stenosis (most common)

Mitral regurgitation

Aortic stenosis

Aortic regurgitation

2. CONGENITAL HEART DISEASES

I NONCYNOTIC

ASD

VSDPULMONARY STENOSIS

COARCTATION OF AORTA

II CYANOTIC

FALLOT’S TETROLOGY

EISSENMENGER SYNDROME

8



Miscellaneous

• Mitral valve prolapse

• Cardiac arrythmias

• Peripartum cardiomyopathy

• Ischemic heart disease• Marfan syndrome

9



Heart disease in pregnancy

• The overall incidence of serious heartdisease complicating pregnancy isapproximately 1%.

• During the last few decades, theetiology of heart disease in developedcountries has changed from primarilyrheumatic to predominantly congenital

(JAMES HIGH RISK 4th ed)

10



Incidence in India

According to a study carried out in anIndian medical institute, the incidenceof heart disease in pregnncy wasestimated to be 1.3%. This study

indicated that rheumatic heart diseasewas the commonest heart condition(78%) of which mitral stenosis was thecommonest heart defect (71.54%).

Congenital heart disease (18.7%) is thesecond most common heart condition inpregnancy.

(https://www.quest4health.com)

11

https://www.quest4health.com/imported/Heart-Diseases&sub=Pregnancy-related-Heart-Complications?q=imported/























































































































































NYHA Classification of HeartDisease

• Class I. Uncompromised—nolimitation of physical activity

• Class II. Slight limitation of

physical activity• Class III. Marked limitation of

physical activity

• Class IV. Severelycompromised—inability toperform any physical activitywithout discomfort

( WILLIAMS 23rd ed) 12



Predictors of cardiac complications basedon scoring system (2001)

• Prior heart failure, transient ischemicattack, arrhythmia, or stroke.

• Baseline NYHA class III or IV orcyanosis.

• Left-sided obstruction defined asmitral valve area less than 2 cm2, aorticvalve area less than 1.5 cm2, or peak left

ventricular outflow tract gradient above30 mm Hg by echocardiography

• Ejection fraction less than 40 percent

(Williams 23rd ed)

13



Indicators of Heart DiseaseDuring Pregnancy

Symptoms

• Progressive dyspnea or orthopnea

• Nocturnal cough

• Hemoptysis• Syncope

• Chest pain

14



Clinical Findings

• Cyanosis

• Clubbing of fingers

• Persistent neck vein distension

• pansystolic murmur grade 3/6 ,latesystolic,louder ejection systolic

• Diastolic murmur

• Persistent split second heart sound.

( WILLIAMS 23rd ed.)

15



INVESTIGATIONS

ECG:Arrhythmias,biatrial enlargment &24-hour ECG monitor may be indicatedif rhythm disorder suspected

Chest x-ray:cardiomegaly,prominentvascular markings.

ECHO:Structural abnormalities,Flowgradients etc.

Cardiac MRI :Can delineate complexanatomy when not evaluated by echo

16



complications of cardiac diseasein pregnancy

• Maternal effects:depends up on etiology,typeof lesion,functional status,antenatal care andcan 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

• Arrythmias 17



• Congestive cardiac failure occurs at 6-8wks,30-34 wks,2nd stage oflabour,immediate post partum,5dayspost partum,5 months after delivery.

• Acute rheumatic carditis seen in 1st trimester

• Subacute bacterial endocarditis occurs

In 1% & should be suspected if patienthas fever,rapid hemodynamicdeterioration,& leukocytosis without anysource of infection

18



• Chances of embolism more inimmobilised patients & with prostheticvalves &cardiomyopathy

19



Mortality associated

Low risk of maternal mortality (lessthan 1%).

(a) Septal defects.

(b) New York Heart Associationclasses I and II.

(c) Patent ductus arteriosus.

(d) Pulmonary / tricuspid lesions.

( DE SWIET 5th ed)

20



Mortality associated………CONT

Moderate risk of maternal mortality (5-15%).

(a) NYHA classes III and IV mitralstenosis.

(b) Aortic stenosis.

(c) Marfan’s syndrome with normalaorta.

(d) Uncomplicated coarctation ofaorta.

(e) Past history of myocardialinfarction.

REF.DE SWIET 21



High risk (Mortality 25-50%)

• Pulomonary hypertension

• Eisenmenger syndrome

• Severe aortic stenosis

• Marfan syndrome with aortic rootdilatation or major valvular involvement.

• COA with valvular involvement

22



Maternal prognosis

• Pregnancy does not affect survival afterpregnancy

• Prognosis becomes clear at 28-32 wks

• In subsequent pregnancy tendency tofall in lower functional class

23



Fetal effects

• Miscarriage

• Prematurity

• Fetal growth restriction

• Increased congenital malformations(3-10%)

• Fetal death

24



Fetal prognosis

• In RHD prognosis good though perinatalmortality slighty more and birth wt onaverage 200gms less than for normalpatients

• Chances of pre term in case of advancedisease

• In case of congenital diseases poorprognosis & depends up on degree of

cyanosis• Chances of fetus being affected is 2-3%

if father affected & 5-6% if motheraffected

25



General management principles

• Aim is prevention,early diagnosis,

appropriate treatment

All women should be counselled before

pregnancy.Women with contraindications advised notto conceive

Those with valvular lesions should conceive

when they are in NYHA class I&IIThose with severe disease eg severe MSshould undergo surgery beforepregnancy

26



Indications for MTP

• ABSOLUTE

• Eisemenger’s syndrome

• Primary pulmonary hypertension

• Single ventricle• marfan’s syndrome with aortic root

diameter>7cm

• Peripartum cardiomyopathy

• Pulmonary veno occlusive disease

27



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&EBefore 12wks preferably 8wks

28



Ante natal care

• OBJECTIVE: To minimise factors that encroachup on limited circulatory reserve

• Should be seen regularly by cardiologist &Senior obstetrician

• Counsel about specific lesions ,functional cardiacstatus,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

29



• Careful vigilance for preeclamsia

• Early diagnosis & treatment ofUTI,RTI,dental infection.

•All women with RHD should receive• Pencillin prophylaxis(benzathine pen.1.2mega units)or erythromycin if patientallergic 250mg BD throughout pregnancy

• Fetal monitoring routine USG, fetalECHO, NST,BPP.

30



INDICATIONS FORADMISSION

• Women with class III&IV should beadmitted when diagnosed untill deliveryor functional status improves

• Class I&II admitted 2wks prior toexpected date of delivery

• Worsening of cardiac status

• Cardiac failure

• Appearnce of symptoms & sign likecough, dysnea,basal lung crepitations

31



Management of labour anddelivery

• Generally vaginal delivery best

• induction best avoided unless obstetricindication

• Casearean for obstetric indication

• INDICATIONS FOR CESAREAN

• Obstetric indications

• Large aortic aneurysm

32



Management of first stage oflabour

• Semirecumbent position with lt. lateral tilt• i/v fluids restricted to 75ml/hr except inAS

• 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

• Basal cre itations33



i/v Prophylactic antibiotics

34



• Invasive monitoring by PAC in high riskcases.

SECOND STAGE MANAGEMENT

Cutting short 2nd stage not in every case

When required than by forceps or vaccum

35



Third stage management

• Oxytocin 10 units i.m. except in lt. to rt.Shunts or sever outflow obstruction

• Avoid methergin

• Misoprost can be given

36



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

37



contraception

• Barrier methods

• POPs can be given

• DMPA good option• IUCD relatively contraindicated

• Ocps contraindicated

• Vasectomy of husband , mini laprotomyLaproscopic sterlisation not advisable

38



Management of complications

CONGESTIVE CARDIAC FAILURE

• Bed rest

• Salt intake restriction

• Diuretics 40-80mg i/v frusemide f/b40mg daily

• Serum potassium monitoring daily

39



Management of arrythmias

• Digoxin drug of choice .25mg i/v every2hrs 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 individed doses.

• Cardioversion in chronic &hemodynamically unstable patients

• Anticogulation in chronic arrythmias• Other drugs -

esmolol,metoprolol,propranol verapamil

40



Management of acute pulmonaryedema

• Propped up position

• Oxygen inhalation

• Morphine 5mg i/v repeated 5-10 minutesup to maximum dose of 15mg.

• Diuresis with frusemide

• Monitorning of oxygen saturation

41



Infective endocarditis

• Admit patient

• Antibiotics

• Pencillin G 10-20 m units i.m/i.v and

gentamicin 1.5mg/kg body weight 8hrlyfor 2wks

vancomycin 15mg/kg i/v 12hrly 4wks

watch for CCF & treat accordingly

Maternal mortality 20-25%

42



Surgical and percutaneousinterventions in pregnancy

CLOSED MITRAL VALVOTOMY

• Can be carried out at any stage

Indications-

• Failure of medical therapy withintractable symptoms

• Profuse haemoptysis

• History of pulmonary edema before

pregnancyProvided-

No calcification of valve

No associated MR43



Balloon valvuloplasty

It has replaced valvotomy

Prerequisits are-

Non calcified valve

No major MR

Done between 24-28wks

COMPLICATIONS-

Acute MRProcedural tamponade

Thromboembolism

Only <2%44



Mitral valve replacement

• Although usually postponed until afterdelivery, valve replacement duringpregnancy may be lifesaving in case of lifethreatening pulmonary edema.

• Maternal mortality 1-5%• Fetal mortality 20-33%

• it is recommended that surgery is doneelectively

• pump flow rate is maintained 2.5 L/min/m2,

• normothermic perfusion pressure is 70 mmHg,

• hematocrit is 28 percent.45



Choice of valve

• Porcine tissue valves are much saferduring pregnancy, primarily becauseanticoagulation is not required asthrombosis is rare .

• To the contrary, valvular dysfunction,deterioration,or failure are common, anddevelop in 5 to 25 percent

• Another drawback is that bioprostheses

are not as durable as mechanical ones,and valve replacement averages every 10to 15 years.

46



CORRECTION OFCONGENITAL DEFECTS

INDICATIONS-

• Fast worsening symptoms

• Class IV status in early pregnancy

• History of deterioration in previouspregnancy

Best time- 20-24 wks if any choice

47



Pregnancy in women withprosthetic valves

• Mechanical valves and anticoagulation wereassociated with a moderate increase inmiscarriage and thromboembolic events.

• Mechanical valves were associated with a

maternal mortality rate of 3.7 percent and athromboembolic rate of 14.8 percent.

• Thromboembolism was increased fourfold withheparin use rather than warfarin. Mitral valves

accounted for 81 percent of thromboticcomplications.

48



American College of Chest Physicians Guidelinesfor Anticoagulation of Pregnant Women with

Mechanical Prosthetic Valves

• Adjusted-dose LMWH twice daily throughout pregnancy.The doses should be adjusted to achieve the manufacturer’s peak anti-Xa level 4 hours after

subcutaneous injection.• Adjusted-dose UFH administered every 12 hours

throughout pregnancy. The doses should be adjusted to keep the midinterval aPTT at least twice control or attainan anti-Xa heparin level of 0.35 to 0.70 U/mL.

• LMWH or UFH as above until 13 weeks’ gestation withwarfarin substitution until close to delivery when LMWHor UFH is resumed

49



•INDIVIDUAL

LESIONS

50



1. mitral stenosis

Rheumatic endocarditis causes threefourths of mitral stenosis cases.

• In a 12-year review of 486 pregnantpatients in India through 1999, 63%of lesions affected a single valve.Mitral stenosis was the abnormality in90% of these women

(JAMES 4th ed)

51



CONT….

The normal mitral valve surface area is

4 -6 cm2. When less than 2.5cm2,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 afterage 30.

• Rapidly progressive in the natives of

developing world so one should have ahigher index of suspicion

• Mitral stenosis restricts leftventricular inflow, with resultant

elevation of the left atrial andpulmonary venous pressures.

DE SWIET 5th ed53



MS CONT .

The diagnosis is made onechocardiography and classified asfollows:-

mild 1.5–2.0 cm2

moderate 1–1.5 cm2

severe <1.0 cm2.

de swiet 5th ed

54



Cardiac examination:-

• may reveal a loud S1 (S1 is as loud orlouder than S2 when listening over theaortic or pulmonary area)

• opening snap (a sound heard shortly

afterS2)• a diastolic rumbling murmur

• signs of right ventricular strain andpulmonary hypertension may become

apparent

• de swiet 5th ed

55



Ms cont.

• Patients with mild-to-moderate oroccult mitral stenosis may firstbecome symptomatic during pregnancy.

• Increased volume and heart rateadversely affect cardiovascularhemodyanmics in rheumatic mitralstenosis clinical deterioration during

gestation should be expected.

56



MS CONT.

• The flow of blood from the leftatrium to the left ventricle duringdiastole 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 orequal to 2.5 cm2.

• Symptoms at rest are expected atless than or equal to 1.5 cm2.

GABBE 5th ed57



MS CONT.

• The left ventricle responds with Starling mechanisms to increasedvenous return with increasedperformance, elevating CO in response

to demand.• The left atrium is limited in its

capacity to respond. Therefore, CO islimited by the relatively passive flow

of blood through the valve duringdiastole.

Increased venous return results inpulmonary congestion rather than

increased CO.58



MS CONT…………

• The relative tachycardia experiencedin pregnancy shortens diastole,decreases left ventricular filling, andtherefore, further compromises CO

and increases pulmonary congestion.

59



DIAGNOSIS

• Diagnosis in pregnancy beforematernal decompensation is uncommon.

• Tiredness and dyspnea on exertion arecharacteristic symptoms of mitral

stenosis. • Hemodynamic tolerance is generally

good during the first trimesterbecause tachycardia and increase in

cardiac output are still moderate.• Symptoms generally begin during the

second trimester

Celia Oakley 2nd ed.60



DIAGNOSIS CONT……

• Theoretically, clinical diagnosis shouldbe easier during pregnancy becausethe intensity of the murmur tends toincrease with cardiac output. but

perception of the murmur may bedifficult because of tachycardia

• Intercurrent event such as a febrileepisode will result in exaggerated

symptoms• Under these circumstances,

echocardiogram should be performedto rule out mitral valvular disease.

61



Diagnosis………

• Echocardiographic diagnosis of mitralstenosis is based on the characteristicappearance of stenotic,frequentlycalcified valve

• Calculation of valve area frompressure half-time of the Dopplerwave or by two-dimensional planimetryprovides an objective measure of

severity.

Gabbe 5th ed

62



MANGEMENT OF MS

• PREPREGNANCY

•ANTE NATAL

• INTRAPARTUM

• POSTNATAL

63



PRE PREGNANCY• The goal of preconception care is to

define the severity of cardiaccompromise

• Two-dimensional echocardiography andcolor-flow Doppler are used todetermine cardiac function and thedegree of stenosis

• In symptomatic patients or those withseverely stenotic valves, surgicalcorrection should be done beforeconception

• Surgical commissurotomy/Percutaneousmitral valve commissurotomy

• james 4th ed64

ANTEPARTUM



ANTEPARTUM• The goal of antepartum care is to

achieve a balance between the driveto increase CO and the limitations offlow across the stenotic valve.

• Limited physical activity

• If symptoms of pulmonary congestiondevelop:-

activity is further reduced,

Dietary sodium is restricted

Diuretic therapy is started• B-blockers usually given to blunt the

cardiac response to activity andanxiety

65



CONT.

• If new-onset atrial fibrillationdevelops,intravenous verapamil, 5 to10 mg, is given, orelectrocardioversionis performed.

• For chronic fibrillation, digoxin, B -blocker,or a calcium-channel blockeris given to slow ventricular response.

• Therapeutic anticoagulation with

heparin is indicated with persistentfibrillation

66



CONT.

• Serial echocardiography is indicatedto follow cardiac function.

• Percutaneous mitral balloonvalvulotomy may be necessary to treat

patients with significant functionaldeterioration or refractory pulmonaryedema, despite optimal medicalmanagement.

• Women with a history of Rheumaticvalvular disease should receiveprophylaxis with daily oral penicillin Gor monthly benzathine penicillin.

WILLIAMS 23rd ,GABBE 5th,JAMES 4th ed

67



INTRAPARTUM

• During the intrapartum period, volumestatus and cardiac output are criticalconcerns

• In patients with NYHA class III orIV disease, central hemodynamicmonitoring

• pulmonary Capillary wedge pressure(PCWP) can warn of the potential forpulmonary edema,

• Fluid restriction or careful diuresis,with attention to cardiac output, maybe used to obtain desirable pressures

68



CONT… •

Careful intravenous administration ofβ-blockers

• Epidural analgesia is both safe andeffective.

• Cesarean delivery is typically reservedfor obstetric indications

• Although forceps delivery is advocatedto shorten the second stage of laborand reduce bearing down, it is notalways required

• Endocarditis antibiotic prophylaxisshould be given prior to cesareansection

.JAMES 4th ed69



POSTNATAL

• Postpartum fluid shifts increase therisk of pulmonary edema.

• PCWP increase by 10 mm Hg betweenthe second stage of labor and the

postpartum• Because frank pulmonary edema is

unlikely at a PCWP of less than 30mm Hg, maintaining the PCWP at 14

mm Hg or lower if centralhemodynamic monitoring is employedshould prevent this complication

JAMES 4th ed70

PREGNANCY OUTCOMES



PREGNANCY OUTCOMES• complications are directly associated

with the degree of valvular stenosis

• Canadian study found that women witha mitral-valve area 2 cm2 were atgreatest risk for complications.

• In another study from California on46 pregnant women with mitralstenosis, Complications included heart

failure in 43 percent and arrhythmiasin 20 percent.

williams 23rd ed71



Cont.

• Fetal-growth restriction was morecommon in those women with a mitralvalve area less than 1.0 cm2

• Among 486 pregnancies complicated byrheumatic heart disease predominantlymitral stenosis—Sawhney andassociates reported that eight of 10

maternal deaths were in women inNYHA classes III or IV.

williams 23rd ed

72



Aortic stenosis• Aortic stenosis is the most common

cardiac valve lesion in the UnitedStates.

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 isthe most frequent etiology seen duringpregnancy.

JAMES 4th ed73



CON……

• Aortic stenosis of rheumaticorigin is typically progressive

• Tends to be less severe in

patients of reproductive age.• It accounts for only 5% to 10%

of cases of rheumatic heartdisease in pregnancy

• Usually seen in conjunction withmitral valve disease.

74



CONT….

• The normal aortic valve area is 3 to 4cm2.

• The pressure gradient across thevalve 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 welltolerated in pregnancy, and cardiaccomplications typically do not occur

75



DIAGNOSIS• Young women with aortic stenosis are

usually asymptomatic.• Although they may develop increasing

exercise intolerance in pregnancy, theprogression is insidious and not easily

distinguished from the effects ofnormal pregnancy.

• The diagnosis is usually made by theauscultation of a harsh systolic

murmur.• Diagnos is confirmed by echo

76



HEMODYNAMICS

• Aortic stenosis is a condition ofexcess left ventricular afterload.

• Ventricular hypertrophy increasescardiac oxygen requirement.

• whereas increased diastolicventricular pressure impairs diastoliccoronary perfusion.

Each increases the potential for

myocardial ischemia.

77



Cont.

• The left ventricle requires adequatefilling to generate sufficient systolicpressure to produce flow across thestenotic valve.

• Given a hypertrophied ventricle andsome degree of diastolic dysfunction,the volume-pressure relationship isvery steep

• A small loss of left ventricular fillingresults in a proportionately large fallin left ventricular pressure and,therefore, a large fall in CO.

78



Cont.

• The pregnant patient with significantaortic stenosis is very sensitive to lossof preload associated with hemorrhageor epidural induced hypotension.

• The window of appropriate fillingpressure is narrow

• Excess fluid may result in pulmonaryedema & insufficient fluid may resultin hypotension and coronary ischemia

79



Cont.

• In general, pulmonary edemaassociated with excess preload ismuch easier to manage thanhypotension 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.

81

ANTENATAL



ANTENATAL

• Physical activity should be limited.• Patients should be observed for signs

of congestive heart failure orarrhythmias.

• Serial fetal ultrasounds should bescheduled to detect evidence ofgrowth restriction

• Given that most aortic stenosis in

young women is congenital in origin,fetal echocardiography is indicated.

82



ANTENATAL

• Hospital admission one day beforeplanned induction of labor with afavorable cervix is preferred.

• A prolonged induction should be

avoided.• The patient should be gently hydrated

overnight to achieve a pulmonaryartery wedge pressure (PAWP) of 12

to 15 mm Hg• An elevated PAWP serves as a buffer

against a loss of preload.

83



INTRAPARTUM

• Fluid management is the criticalcomponent 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 adequatevolume loading.

• Use of a PAC may aid in monitoringvolume status in Patients withgradients above 60 to 80 mm Hg

JAMES 4th & GABBE 5th ed84



Cont.

• A narcotic epidural can decrease theoccurrence of hypotension.

• Pulmonary edema – no overaggressivediuresis

• Oxygen supplementation.• morphine

• Dopamine or dobutamine ,maintaincardiac output.

• Bacterial endocarditis prophylaxis isrecommended for cesarean delivery.

JAMES 4th ed

85

POSTNATAL



POSTNATAL

• Postpartum, patients should bemonitored hemodynamically for 24 to48 hours.

• Diuresis is usually spontaneous the

patient can be allowed to find herpredelivery compensated state.

• When diuresis must be induced totreat pulmonary edema, it should bedone gently and carefully.

• Predelivery hemodynamic parametersshould be used as an endpoint

GABBE 5th

ed86

Coarctation of the Aorta



Coarctation of the Aorta

• Coarctation of the aorta results froma constriction of the aorta at orabout the level of the ductusarteriosus or left subclavian artery.

• Patients have a characteristicdiscrepancy in blood pressure between their right arm and lower extremities

• Untreated coarctation of the aortacarries a poor prognosis and isuncommon today.

87

CONT



CONT.• Several cardiovascular anomalies are

associated with coarctation of theaorta.

• A bicuspid aortic valve is the mostcommon, found in (85%) of patients.

• VSDs, anomalies of the intercostal and• subclavian arteries, and aneurysms of

the circle of Willis(69%) may also bepresent.

• Hypertensive disorders of pregnancyarecommon and reported in more than15% of patients.

JAMES 4th DE SWIET 5th ed88



CONT…….

• A systolic or occasionally continuousmurmur can be heard in the

infraclavicular or scapular area

• Some patients will only present laterin life with hypertension

• Delay between brachial and femoralpulses

89



CONT……

• Although data are limited, thephysiologic changes associated withpregnancy may unmask and aggravatepostrepair 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, aorticdissection and rupture

91

Mangement



Mangement• Termination may be considered in

patients with uncorrected coarctationof the aorta

• The majority of patients will have had aprevious repair and require evaluation

• The highest risk of rupture ordissection is in patients with a Dacronpatch repair

• Fetal echocardiogram.

• Ideally, moderate-to-severe aorticcoarctation should be repaired, withballoon angioplasty or stenting, orreplacement prior to pregnancy

92

CONT



CONT.• 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 secondstage to reduce Valsalva, is preferred.

• Increased hypertension and myocardialoxygen demand can be reduced by the

use of beta-blockers• Adequate pain control, particularly with

the use of epidural anesthetics.

93



Pulmonary Stenosis

• Pulmonary valve stenosis is the mostcommon type of isolated rightventricular outflow tract obstruction.

• Almost always congenital in origin.

• Associated with a systolic ejectionmurmur at the left upper sternalborder 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 stenosisshould have percutaneous balloonvalvuloplasty before conception.

• These patients are often left with

some degree of insufficiency,buttolerated well.

• Patients with unrepaired mild-to-moderate pulmonary stenosis(gradients

< 40 mmHg) usually asymptomatic andtolerate the hemodynamic burden ofpregnancy

95



Atrial septal defects• The most common congenital lesions in

adults may be first diagnosed duringpregnancy.

• There are three types• The most common 80%, is the

secundum type.

• The secundum ASD(located in thecentral portion of the atrial septum)is associated with myxomatous mitralvalve disease and prolapse in 20–30%of cases.

96



CONT.

• The more unusual types are:-• Primum, or endoardial cushion, defects (

in the lower portion of the atrialseptum),

• which are most commonly associatedwith Down’s syndrome

• Sinus venosus defects (located in the

upper portion of the atrial septum) in

which the right upper pulmonary vein isusually emptying into the superior venacava and right atrium.

97



• The uncorrected left-to-right shunt

produces a volume load on the right sidewith enlargement of the right atriumand 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 acrossthe pulmonary valve may cause a 2/6

systolic ejection flow murmur.• ASD causes a wide fixed split secondheart sound with the patient in thesitting/standing position

98



• Signs of right ventricular hypertrophyand pulmonary hypertension can bepresent 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 ontransthoracic echocardiography but mayneed transesophagealechocardiographyto detect some smaller shunts and sinus

venosus defects.

100

Hemodynamics &Pregnancy



y g youtcome

• The expected 50% increase in bloodvolume during pregnancy causes furthervolume loading,

• Most patients with an isolated ASD

tolerate pregnancy well• ventricular ejection fraction and NYHA

functional status are predictive ofuncomplicated and successful outcomes

101



• With larger defects and shunts, there isrisk for congestive heart failure, atrialarrhythmias, peripheral venousthrombosis

or embolism, cerebral vascularaccidents, and shunt reversal

• Congestive heart failure can be treatedmedically with digoxin and diuretics.

• Atrial arrhythmias can worsen orprecipitate heart failure and should betreated with beta-blockers and digoxin.

102



• low-dose aspirin after the firsttrimester is advocated to reduce therisk of venous thrombosis and henceparadoxic emboli.

• Systemic hypotension, which can occurduring parturition and epiduralanesthesia, should be anticipated andcorrected to prevent possible shuntreversal and oxygen desaturation.

• Preconception closure of the defect isrecommended for women withsymptoms,

arrhythmias or significant right-to-left

shunts where ( Qp / Qs ) is 1.5:1103



VSD

• Ventricular septal defects (VSD) arecommon at birth (0.3–3 /1000 livebirths)but

• Many close spontaneously in childhood

• The size and location of the defectaffect the clinical course.

• The most common type of defect occursin the membranous septum or left

ventricular outflow tract

104



• The flow across a VSD produces a loud(typically 4–6/6) systolic ejectionmurmur

• Clinical sequelae and symptoms are most

likely to happen if the VSD is large• Effects of chronic volume overload and

secondary pulmonary hypertension beginto manifest as exercise intolerance,

dyspnea or congestive heart failure.

105



• Infective endocarditis, however, canoccur with any size of VSD.

• Similarly to ASD, VSD should berepaired if symptomatic or associated

with an elevation in pulmonary arterypressure.

• Isolated VSD are usually well toleratedin 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, noincreased risks

107



Patent ductus arteriosus

• Patent ductus arteriosus is thepersistence after birth of the directconnection between the pulmonary andarterial circulation

• Incidence of Isolated, persistentpatent ductus arteriosus 1:2000newborns, but rarely in adults.

• The residual embryonic shunt is from

the descending aorta at the isthmus tothe proximal left pulmonary artery

108



• Clinical symptoms and complications arealso similar to those associated withVSD.

• Physical examination classically reveals a

grade 4–6/6 continuous(diastolic andsystolic), “machinery” murmur that isbest heard at the upper left sternalborder or infraclavicular area.

• Risks of pregnancy are related to shuntsize and degree of pulmonaryhypertension

109



• In small shunts, maternal and fetaloutcomes are not altered

• Theoretical risk of shunt reversal

• Patients with large shunts have

enlargement of the pulmonary arteryand left-sided chambers and can develophigh-output heart failure.

• In corrected or uncorrected patent

ductus arteriosus, pulmonaryhypertension significantly increasesmaternal and

fetal morbidity and mortality rates110

MITRAL REGURGITATION



• Mitral regurgitation may be due to achronic progressive process such asrheumatic valve disease or myxomatousdegeneration of valve

• Frequently associated with mitral valveprolapse.

• As regurgitation increases over time,forward fl ow is maintained at the

expense of left ventricular dilation witheventual impaired contractility.

111



HEMODYNAMICS

• The hemodynamic changes associatedwith pregnancy can be expected to havemixed effects.

• A reduction in SVRtends to promote

forward flow.• The drive to increase CO will

exacerbate left ventricular volumeoverload.

• Increased atrial dilation may initiateatrial fibrillation

• Pulmonary congestion

112

Preconceptional counseling



Preconceptional counseling

• valve replacement in consultation with

• a cardiologist. In general valvereplacement is recommended for:-

• symptomatic patients• atrial fibrillation

• ejection fraction less than 50 to 60percent

• left ventricular end-diastolic dimensiongreater than 45 to 50 mm, or

• pulmonary systolic pressure greaterthan 50 to 60 mm Hg.

113

L b & D l



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 pulmonarycongestion.

• Insufficient preload will not fill theenlarged left ventricle and will result ininsufficient forward flow

114

M



Manag…….

• A pulmonary artery catheter can beused to determine appropriate fillingpressure in early labor or beforeinduction.

• The pulmonary artery diastolic pressurecan be used as a reference point.

• Diuresis in the early postpartum period

• may be required.

• Acute mitral regurgitation uncommonand may be associated with rupturedchordae tendineae due to endocarditisor myxomatous valve disease.

115

M



Manag……..

• Without time for left ventricularcompensation, forward flow may beseverely compromised.

• Urgent valve surgery is usually required.

• Inotropic left ventricular support andsystemic after load reduction can be

used to stabilize the patient.

116

AORTIC REGURGITATION



• Aortic regurgitation is most often dueto:-

• A congenitally abnormal valve

• Marfan’s syndrome

• Endocarditis• Rheumatic disease

The reduction in vascular resistanceassociated with pregnancy tends to

improve cardiac performance

117

MANAG



MANAG…..

• Valve replacement is generallyrecommended for:-

• (1) (NYHA) functional class III andclass IV symptoms

(2) an ejection fraction less than50 percent

(3) left ventricular end-systolicdimension greater than 55 mm

118



• Labor and delivery is managed withstandard cardiac care.

• Pulmonary artery catheterization is notusually required.

• As the hemodynamic changes associatedwith pregnancy resolve, a rise in vascularresistance should be anticipated andafter load reduction maintained.

119

Ebstein’s anomaly



Uncommon congenital heart lesion, amalformed tricuspid valve is apicallydisplaced to a variable extent with:-

• Tricuspid regurgitation

• Atrial dilation• Limited right ventricular function

• Severe cases present in infancy, butmany cases will first present in teenager

or adults.• Complications include CHF, arrhythmias,

and paradoxic embolism

120



Associated abnormalities are frequent• Include ASD (50%) and Wolff

Parkinson–White (WPW) syndrome(30%)

• Most patients can be treated medically• More severe forms may develop right

heart failure and require surgicalcorrection

121



• Preconception repair is preferable,particularly for patients with aninteratrial 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

122



• Complications include CHF, arrhythmias,and paradoxic embolism

• Atrial arrhythmias may occur

• In the presence Wolf-Parkinson White

(WPW)syndrome, atrioventricularconduction can become exceedinglyrapid with resultant hemodynamiccollapse

123

Tetralogy of Fallot• The most common cyanotic congenital



• The most common cyanotic congenitalheart defect found in children, adults,

and pregnant women• It occurs in 3.9 per 10,000 births and

accounts for up to 10% of congenitalheart disease.

• The four diagnostic abnormalities are• VSD

• Deviation of the aorta to the right sothat it over-rides the VSD,

• Infundibular pulmonic stenosis• Secondary right ventricular hypertrophy

de swiet 5th124

• Preconception repair is preferred



• Repair usually involves relief of the

right ventricular outflow obstruction &closure of the VSD.

• corrected patients should have apreconception functional assessment tofurther define risk.

• Patients with corrected lesions, goodresidual right ventricular function andgood functional status usually toleratethe increased hemodynamic stress of

pregnancy.• Prophylaxis with aspirin to reduce

• the risk of thrombosis and paradoxicemboli may be indicated 125



• Prophylaxis with aspirin to reduce therisk of thrombosis and paradoxic embolimay be indicated

• Uncorrected lesions can be expected to

have clinical deterioration duringpregnancy, resulting in increasedmaternal and fetal complications

de swiet 5th ed

126

TRANSPOSITION OF THEGREAT VESSELS



• Transposition of the great vessels (TGV)is present in only 5 percent of pregnantwomen with congenital heart disease

• In complete TGV the aorta arises from

the right ventricle and the pulmonaryartery arises from the left ventricle

• venous blood returns to the rightatrium, and passes through the tricuspid

valve, into the RV, and directly into thetransposed aorta

127



• TGV was first definitively corrected in1964 with the Mustard operationa

• Off late direct surgical switchbetween the pulmonary artery and the

aorta has been performed.• The hemodynamic changes of pregnancy

will have a mixed impact on a patientwith a Mustard repair.Increased CO

increases the volume load on the rightheart. and decreased vascularresistance reduces afterload on theright side of the heart

128



• In surgically corrected patientscomplications that should be anticipatedinclude :-

• CHF due to limited cardiac reserve,

• Tachyarrhythmias• Paradoxic emboli

• The fetal prognosis remains poor, withmortality close to 50% and prematurity

and intrauterine growth restrictionranging from 30% to 50%

• GABBE 5th & DE SWIET 5th

129

Evaluation before pregnancy should



• Evaluation before pregnancy shouldinclude:-

• Assessment of functional status• Evaluation of heart function

• Confirmation of normal oxygenation.

• When the right side of the heart is thesystemic heart, pharmacologic afterloadreduction should be maintained untilpregnancy is confirmed.

• Young women with surgically correctedTGV can be expected to successfullycomplete pregnancy

GABBE 5th ed130

Eisenmenger’s syndrome



Eisenmenger s syndrome

• Severe pulmonary vascular obstructivedisease and hypertension resulting fromseptal communication between thesystemic and pulmonary circulations is

termed Eisenmenger’s syndrome.• Eventually the normally “ lowerpressure” right ventricle and pulmonarycirculation begin to see pressures thatapproach the pressures on the normally“ higher pressure” left heart.

131



Pulmonary hypertension



y yp

• Although pulmonary hypertension isfundamentally a pulmonary disease, themajor pathologic impact is on the rightside of the heart.

• The incidence of primary pulmonaryhypertension is 1 to 2 per 1 million, with

women affected more commonly thanmen.

• The reported mortality of PH hasranged from nearly 60% in earlyreports, to as low as 25% more recently.

( Clin Chest Med 32 (2011) 165–174&Gabbe)133



• Secondary pulmonary hypertension may

develop as a complication of cardiacdisease such as mitral stenosis orsecondary to intrinsic pulmonarydisease.

• Drugs such as cocaine or appetitesuppressants may also be associatedwith pulmonary hypertension.

• The maternal mortality with severe

pulmonary hypertension is reported tobe as high as 50 percent.

• Sudden, irreversible deterioration inthe postpartum period is common.

Gabbe 5th

ed

134

Physiology



Physiology

• patients with preexisting PAH areunable to make adjustment to pregnancyinduced cvs changes.

• The right ventricle, which now faces

increased afterload from higher PVR,cannot accommodate the increase incardiac output and becomes overloaded.

• This can result in progressive right

ventricular failure and sudden deathfrom arrhythmia.

135



• The pain of parturition is associatedwith stimulation of the sympatheticnervous

system and dramatic increases in heart

rate, blood pressure, and myocardialoxygen consumption,and can beassociated with vagal responses that canlead to hypotension and sudden death.

136



Updated clinical classification ofpulmonaryhypertension (Dana Point)



hypertension (Dana Point)

• Class 1: Pulmonary Arterial HypertensionIdiopathic

• Class 2: Pulmonary Hypertension Causedby Left side Heart Disease

• Class 3: Pulmonary Hypertension Causedby Lung Disease and/or Hypoxia

• Class 4: Chronic ThromboembolicPulmonary Hypertension (CTEPH)

• Class 5: Pulmonary Hypertension withUnclear Multifactorial Mechanisms

Clin Chest Med 32 (2011) 165–174

138

DIAGNOSIS AND SCREENING



• The symptoms of pulmonaryhypertension are nonspecific.

• Increasing fatigue and shortness ofbreath 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 mustbe confirmed by RHC

139

PREGNANCY OUTCOMES ANDMORTALITY &MANAGMENT



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 rightventricular performance.

• Pharmacologic treatment with nifedipineor intravenous prostacyclin may also beeffective.

140



• Anticoagulation with heparin should beconsidered.

• Worsening disease will usually bemanifest by falling CO rather than

rising right ventricular pressure.• Labor and delivery should be managed

with standard cardiac care, withparticular

attention to right ventricular filling asassessed by measurement of centralvenous pressure (CVP)

141



• Women with pulmonary hypertension andright ventricular dysfunction should bestrongly discouraged from becomingpregnant.

Gabbe 5th edition

142

Peripartum cardiomyopathy



• Peripartum cardiomyopathy is a rare

syndrome• Although rare, cardiomyopathy in

pregnancy accounts for a significantproportion of maternal deaths

• Mortalities have ranged as high as18%to 56%

143

INCIDENCE



INCIDENCE

• The incidence with rates ranging fromapproximately 1:15,000 pregnancies inthe United States to as frequent as1:299 in a well-studied population inHaiti and 1:100 in a small region of sub-Saharan Africa.

144

Diagnostic Criteria forPeripartum Cardiomyopathy



Peripartum Cardiomyopathy

• 1. Heart failure within the last monthof pregnancy or 5 months postpartum

• 2. Absence of prior heart disease

• 3. No determinable cause

• 4. Echocardiographic indication of leftventricular dysfunction:-

• Ejection fraction <45 percent orfractional shortening <30 percent

• Left ventricular end-diastolicdimension >2.7 cm/m2

GABBE 5th edition

145

Risk factors include:-



Risk factors include:

• Hypertension

• Preeclampsia

• Multiparity

• Multiple gestations• African descent

• older maternal age

146

PATHOGENIC MECHANISMS



PATHOGENIC MECHANISMS

• Investigation of the pathophysiology hasbeen limited by the rare incidence

• For many years it was believed thatPPCM was a variant of IDCM

• PPCM is its own distinct entity

147

PATHOPHYSIOLOGY



PATHOPHYSIOLOGY

148

Int J Cardiol2009;131:168–79;

ecommen e t erapy orPPCM • Goals



G a

• Treat hypertension

• Fluid restriction

• Dietary salt restriction

• Routine exercise post partum if stable

• Drugs for routine use• Diuretics

• b-Blockers

• Vasodilators

• Digoxin

149

Therapies in selected patients • Inotropes



Inotropes

• Anticoagulation

• Implantable defibrillators

• Biventricular pacing

• Cardiac transplantation

150



• Serial clinical assessment should beperformed at each return visit

• assessment of ejection fraction and

structural heart changes should be

performed in patients who have had achange in clinical status

• Serial measurements of BNP to guidetherapy

• Serum electrolytes and renal functionshould be monitored frequently

151



• A sonogram at 20 weeks’ gestation toassess fetal anatomy, then serially toassess fetal growth

• Antenatal testing (nonstress test and

biophysical profile) starting at 32 weeksand then weekly thereafter

• Fett recently proposed a focusedmedical history test for PPCM patients

duringthe latter portion of the pregnancy andpost partum period.

152

Evaluating for:-

• orthopnea



• orthopnea,

• dyspnea,• unexplained cough,

• lower extremity swelling,

• excessive weight gain

• PalpitationsTests for natriuretic peptide levels andhigh-sensitivity CRP (hs-CRP) areperformed if the patient has 3to 4

points or more, with repeatechocardiography if these are increased

153

MANAGEMENT OF DELIVERY• If medical management is successful in

st bili in p ti nt ith PPCM th n l



stabilizing a patient with PPCM, then early

delivery is not required and spontaneouslabor is not contraindicated

• Labor induction can be conducted withminimal risk and, if cervical ripening isrequired:-

• prostaglandins

• oxytocin

• Avoid fluid overload

• Shortening the second stage of labor withthe use of low forceps or a vacuum device isrecommended to minimize ventricular work

154



• Cesarean delivery for obstetricindications

• We reserve invasive monitoring forindividuals in whom volume status is

problematic.• Thromboprophylaxis

• Strict monitoring of fluid status

• Diuretic therapy after delivery

• The parturient should be seen 1 weekafter delivery to assess hercardiovascular status

155

MARFAN’S SYNDROME



• an autosomal dominant genetic disordercaused by an abnormal gene for fibrillinchromosome 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, andarachnodactyly.

156



• Diagnosis is usually based on familyhistory, and physical examination,including ocular, cardiovascular, andskeletal features.

• Untreated, life expectancy is reducedby a third, with the majority of deathsdue to aortic dissection and rupture.

• elective repair has been recommendedwhen the aortic root diameter measures5.5 to 6.0 cm.

157



• The predicted diameter for youngadults can be calculated:

• ADpredicted = 1.02 + (0.98 .bodysurface area [BSA]).

• A ratio of less than 1.3 with a dilationrate of less than 5 percent/y suggests alow risk for a cardiovascular event.

• Maternal mortality rate associated with

Marfan’s syndrome in pregnancy inexcess of 50 percent

• studies suggest that women with milddisease, an AD less than 4.0 cm

158



• Women with ADs greater than 5.5 cmshould certainly be counseled to havegraft and valve replacement beforepregnancy

159



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, andpreeclampsia.

• Most myocardial infarctions occur

during the third trimester in womenolder than 33 year & multiparous

161



• Maternal mortality is highest in theantepartum and intrapartum periods.

• 5% to 7% case-fatality rate in womenwith pregnancy-associated AMI

• Therapy modified in the pregnancy• Thrombolytic agents increase the risk

of maternal hemorrhage substantially(8%)

• Used in situations in which cardiaccatheterization facilities are notavailable

162



Anesthetic concerns for pregnantwomen with cardiac disease



• Regional analgesia & anasthesia exceptmost severe disease

• Manipulate timing of anticoagulant drugsto allow a “window” and minimize

concerns about spinal hematoma• Slow, cautious, incremental onset ofregional block is essential

164



• Important points to consider withepidural analgesia in labor include thefollowing:-

• Bupivacaine 0.1% with fentanyl 2–4

g/mL.• Minimize aortocaval.

• Inject local anesthesia in a slow,incremental fashion.

165

Anesthesia for cesarean section

• There is no evidence available to support



There is no evidence available to supporteither regional or general anesthesia asbeing 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 forCS are as follows:-

• Avoid the catecholamine rise associatedwith endotracheal intubation andextubation.

• Neonate less likely to require ventilatorysupport

166

General anesthesia for CS• Involve a cardiac anesthesiologist

A id h l i



• Antacid prophylaxis

• Intraoperative transesophageal echocardiography(TEE).

• Arterial line usually helpful.

• Position mother with a 15° lateral tilt.

• Use GA technique that will minimizecardiovascular changes.

167

The disadvantages of GA forCS



• 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

168



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heart disease complicating pregnancy

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