Cardiac Disease In Pregnancy

CARDIAC DISEASE IN PREGNANCY Dr. K. N. Georgewill Department of Obstetrics and Gynaecology, UPTH.

SYNOPSIS – INTRODUCTION – HEMODYNAMIC CHANGES IN PREGNANCY – SYMPTOMS OF HEMODYNAMIC CHANGES THAT MIMIC CARDIAC DISEASE – CLASSIFICATION OF CARDIAC DISEASES – BURDEN OF HEMODYNAMIC CHANGES ON THE CARDIAC PATIENT**

INTRODUCTION Cardiovascular disease is the most important non-obstetric cause of disability and death in pregnant women, occurring in 0.4 – 4% of pregnancies. It is not surprising that the added hemodynamic burden of pregnancy, labour and delivery can aggravate symptoms and precipitate complications in a woman with pre-existing cardiac disease. Many of these women may be able to sustain a successful pregnancy, but in specific situations, potential risks may arise and should be anticipated.

HEMODYNAMIC CHANGES OF PREGNANCY, LABOUR & DELIVERY The major cardiovascular changes that occur during pregnancy include: ▲Blood volume (25 – 50%) = Plasma vol + RBC mass ▲Plasma vol (30 – 50%): Na+ and fluid retention by the action of progesterone, rennin, aldosterone and prolactin ▲ RBC mass (20 – 40%) Plasma vol > RBC mass = dilutional anaemia ▲Cardiac output (30 – 50%) = ▲stroke vol + ▲ heart rate = ▲myocardial contractility

▲stroke vol (10%) ▲Heart rate (10 – 20%) ▼Peripherial vascular resistance (30 – 50%): due to vasodilatation (oestrogen, progesterone, PgE2, PgI2) and placenta acting as an arteriovenous shunt Blood pressure: systolic is unchanged; diastolic ▼in 1st and 2nd trimester but ▲in 3rd trimester, returning to the non-pregnant state In multiple pregnancy there is ▲▲ in these physiologic variables mentioned above

Additional hemodynamic changes occur during the various stages of labour & delivery & include: ▲cardiac output (20%) with each uterine contraction. Pain, fear & anxiety contribute further to an increase in cardiac output. ▲systolic blood pressure with each contraction, increasing the load on the left ventricle by 10%, while the heart rate falls. Both the blood pressure and cardiac output are ▼ during epidural analgesia in labour Oxytocic drugs can produce further hemodynamic changes

Following delivery, in the absence of post-partum haemorrhage, the cardiac output & plasma vol increase by 20 – 60% due to shift of blood from the uterus & placenta into the vascular space as well as resorption of interstitial fluid The hemodynamic changes of normal pregnancy can result in symptoms & signs that mimic those of heart disease, often making it difficult to differentiate the two. It is therefore, the severity & persistence of symptoms that suggest underlying organic heart disease. Eg

SYMPTOMS OF HEMODYNAMIC CHANGES THAT MIMIC CARDIAC DISEASE Palpitation: ▲HR, SV Dyspnea, shortness of breath, orthopnea: hyperventilation from ▲progesterone, ▼alveolar CO2 tension, upward displacement of diaphragm Easy fatigability: ▲cardiac output at rest Epigastric pain, bloating, heartburn: displacement of diaphragm , stomach & liver by enlarging uterus, ▼GIT motility Dizziness, syncope: ▼venous return due to compression of IVC by enlarging uterus Heat intolerance, sweating & flushing: ▲cutaneous blood flow & ▲metabolic rate

Bounding pulse: ▲cardiac output, ▼peripherial resistance, widened pulse pressure, ▲cutaneous blood flow Widely split S1 & S2: ▲cardiac output, ▲veneous return, delayed right ventricular emptying Third heart sound: ▲cardiac output, rapid ventricular filling Systolic murmur (precordial or left sternal edge): ▲cardiac output, ▲veneous return, ▲mammary flow, turbulent flow through pulmonary valve Varicose veins: incompetent valve following obstruction of IVC, ▲venous distensibility Edema ( legs occasionally hands & face): ▲venous pressure in legs following obstruction of IVC

CLASSIFICATION OF CARDIAC DISEASES CONGENITAL – Left to right shunt (volume overload) Atrial septal defect Ventricular septal defect Patent ductus arteriosus Truncus arteriosus – Obstructive lesions of the outflow tract (pressure overload) – Bicuspid aortic valve stenosis – Pulmonary valve stenosis – Coarctation of the aorta

– Cyanotic heart disease Tetralogy of fallot Eisenmenger’s complex Transposition of the great vessels Ebstein’s anomaly Complex cyanotic heart disease ACQUIRED – Rheumatic/Valvular heart disease Mitral stenosis / regurgitation Aortic stenosis / regurgitation Tricuspid valve disease

– Myocardial disease Cardiomyopathy Ischaemic heart disease Myocarditis – Pericardial disease Acute pericarditis – Infective endocarditis – Arrhythmias Supraventricular Ventricular – Aortic dissection

NEW YORK HEART ASSOCIATION CLASSIFICATION OF DEGREE OF FUNCTIONAL DISABILITY OF CARDIAC DISEASE

Class I: Asymptomatic with normal activity Class II: Slightly symptomatic with normal activity but asymptomatic at rest Class III : Markedly symptomatic with less than normal activities but asymptomatic at rest Class IV: Symptomatic at rest or with minimal activity

BURDEN OF HEMODYNAMIC CHANGES ON THE CARDIAC PATIENT ▲in cardiac output & stroke vol increase preload on the heart. Augmented preload may not be tolerated by obstructive cardiac lesions, such as mitral or aortic stenosis. In the setting of pulmonary hypertension, this additional blood volume and preload burden could result in right-sided heart failure. A decrease in afterload (systemic vascular resistance) from vasodilation in a woman with aortic stenosis may further increase the gradient across the aortic valve, adding to the left ventricular work – left heart failure

Conversely, certain lesions may benefit from the afterload reduction, such as mitral regurgitation and aortic insufficiency. Regurgitant murmurs may soften and the echocardiographic severity of regurgitation decrease during pregnancy. During labour, the augmented preload may exacerbate certain cardiac problems. Often the left-lateral position is recommended for labour, this may prove deleterious (augmented preload) for patients with certain types of cardiac lesions.

VENTRICULAR SEPTAL DEFECT & PREGNANCY The ventricular septal defect is the most common congenital heart disease anomaly identified at birth Less common in adults & therefore in pregnant women b/c they tend to close spontaneously b/4 the women reach adulthood Women with small – moderate sized V.S.D tolerate pregnancy well, although they are at risk of infective endocarditis, Such women generally require antibiotic prophylaxis With large V.S.D, the risk of pulmonary hypertension increases progressively with pregnancy Late complications of V.S.D: ventricular arrhythmias, aortic insufficiency, heart block, sudden death

MITRAL STENOSIS & PREGNANCY Most common type of RHD in young women Most patients with mild – moderate M.S tolerate pregnany well Those with severe disease are likely to dev complications (pul. venous congestion or frank pul. edema, rt ventricular failure, pul hypertension hemoptesis, thromboembolism, atrial fibrillation) Patients with any degree of M.S can dev complications during pregnancy Symptoms can be aggraviated by associated anaemia & tarchycardia resulting from anxiety, fear & stress

The risk of developing heart failure increases progressively throughtout pregnancy & is further increased during labour & delivery & immediately postpartum. The risk of infective endocarditis remains throughout pregnancy, delivery & early puerperium The mortality rate in pregnant women with M.S is 1% overall & 3 – 4% in those with severe disease

Previously rheumatic heart disease was the most common type of heart disease in pregnant women. Because of advances in the medical and surgical treatment of children born with congenital heart disease, an increasing number of such women reach childbearing age. Therefore, congenital heart disease now represent a larger percentage of cardiac disease encountered in pregnancy. It is important, therefore, that obstetricians understand the late complications of operated or unoperated congenital heart disease in pregnancy. However, it is important to state that the sequelae of rheumatic heart disease still remain a problem in the third world.