Heart diseases in pregnancy. Cardiovascular changes during pregnancy: intravascular volume and...
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Transcript of Heart diseases in pregnancy. Cardiovascular changes during pregnancy: intravascular volume and...
Heart diseases in pregnancy
Cardiovascular changes during pregnancy:
intravascular volume and cardiac output increase by 50%
Decrease in peripheral vascular resistance and blood pressure (endothelium dependent factors)
Physiologic high output (HR 10-20 bpm and ejection fraction – early increase in ventricular wall muscle mass, increased end- diastolic volume, heart is phisiologicly dilatated and has higher contractility))
Peak during the second trimester (20-28)
The increased blood volume serves two purposes. First, it facilitates maternal and fetal exchanges of respiratory gases, nutrients and metabolites. Second, it reduces the impact of maternal blood loss at delivery. Typical losses of 300-500 ml for vaginal births and 750-1000 ml for Caesarean sections are thus compensated with the so-called "autotransfusion" of blood from the contracting uterus
Aortocaval Compression - enlarged uterus compresses both the inferior vena cava and the lower aorta when the patient lies supine cousing reducton in return to the heart and cosequent fall in stroke volume and cardiac output (up to 25 %). Pregnant woment should lie on the side or the pelvis should be rotated - so the uterus drops on the side.
Reduced cardiac uotput is associated with reduction in uterine blood flow, and lower placental perfusion = deceleration in FHR on CTG
Pulmonary vascular resistance like systemic vascular resistance in diminished
PCWP – pulomary capillary wedge pressure is the same, but colloid oncotic pressure is reduced - making pregnant women susceptible to pulmonary oedema
(espessialy if there is increse in cardiac pre- load - i.v. Fluides or increased in pulomnary capillary permeability - preeclampsia)
LABOUR: Futher increase in cardiac uotput ( 15% in the first stage
and 50 % in the second stage) Uterine contractions lead to autotransfusion of 300 – 500
ml of blood into circulation Sympathetic response to pain and anxiety elevates futher
HR and blood pressure After delivery there is immediate rise in cardiac output –
relife of IVC and contracting uterus empties the blood to systemic circulation
Women with cardiovascular disease are most at risk of pulmonary oedema during second satge of labour and immediate postpartum period
Cardiac output returns to normal in 2 weeks.
Symptoms mimicking cardiac disease in healthy pregnant women: fatigue, dyspnea, light-headedness
„Abnormal” cardiac findings in pregnancy: displaced apical impulse, prominent jugular venous pulsations, widely split I and II heart sounds, soft ejection systolic murmur
ECG findings: sinus tachycardia, premature atrial/ ventricular ectopic beats, right/left axis deviation, ST-segment depression, T-wave changes
Echocardiographic findings
Mild increase in left ventricular diastolic dimension with preservation of ejection fraction
Functional tricuspid and mitral regurgitation
Small pericardial effusion
Pathology
Outcomes vary with different cardiac lesions
Ability to tolerate pregnancy depends on : Precence of pulmonary hypertention Functional class – NYHA Heamodynamic significance of any lesion Presence of cyyanosis (arterial oxygen sauration < 80%) High risk of death during pregnancy: Eisenmenger
syndrome, pulmonary vascular obstructive disease, Marfan syndrome with aortopathy, mitral stenosis( pulmonary oedema)
Other complications: heart failure, arrythmias, stroke Fetal complications: spontaneus abortion, premature
birth, IUGR, low birth weight, intrauterine fetal death
Left-to-right cardiac shunts:atrial septal defect, ventricular septal defect,
patent ductus arteriosus The incidence of congenital heart disease in pregnancy is
increasing - beter corresctive surgery in children Higher cardiac output does not increase shunting becouse
of attenuating effect of the decrease in peripheral vascular resistance
Pregnancy, labour and delivery – well tolerated unless pulmonary hypertension exists
Risk of paradoxical embolism! with atrial shunts (patent foramen ovale)
Aortic stenosisLeft ventricular outflow tract
obstruction
Heart failure / ischemia developement in severe stenosis (aortic valve area <1 cm² or transvalvular pressure gradient > 64mmHg)
Hypertrophic and noncompliant left ventricle
Complications with severe stenosis because of restricted ability to increase cardiac output
Management:
Symptomatic aortic stenosis: surgical correction first! then pregnancy
Absence of symptoms does not guarantee good tolerance of pregnancy!
If necessary: baloon valvuloplasty during labor and delivery
Coarctation of the aorta
Associated with: bicuspid aortic valve, aneurysms of the circle of Willis, ventricular septal defects, Turner syndrome
Risk of aortic rupture in the III trimester and during labor if CoA not corrected
If CoA corrected before pregnancy – risk of PIH developement due to residual abnormalities in aortic complience
Pulmonary valve stenosis Classification - according to the peak pressure
gradient across the valve:
mild <50mmHg; moderate 50-70mmHg; severe >80mmHg
Pregnancy well tolerated if stenosis mild or treated by valvuloplasty or surgery
Right-sided heart failure or atrial arrhythmias in severe stenosis (including asymptomatic!)
Management:
Severe pulmonary valve stenosis requires correction before pregnancy
If symptoms progress during pregnancy – baloon valvuloplasty
Tetralogy of Fallot If not corrected/palliated:- fall in systemic vascular resistance and
rise in cardiac outputexacerbate right-to-left shunting
- results: increased maternal hypoxemia and cyanosis
- poor fetal outcomes (loss rate ~30%)- maternal mortality risk 4 – 15%
If succesfully corrected: low risk; pregnancy well tolerated
Marfan syndrome
Connective tissue disorder
Autosomal-dominant
Complications due to medial aortopathy: dilation, dissection, valvular regurgitation
Aortic root replacement before pregnancy does not eliminate the risk of dissection of the residual native aorta!
Management
Recent data: maternal mortality rate: 1%; fetal mortality rate ~ 22%
Aortic root involvement: preconception counseling – risk in pregnancy
Little cardiovascular involvement; aortic root diameter < 40mm – good tolerance of pregnancy
Serial echocardiography to monitor for progressive aortic root dilation
Beta-blockers prophylactically – reduce aortic dilatation
Eisenmenger syndrome & pulmonary vascular obstructive
disease ES: pre-existing left-to-right shunt; pulmonary
pressure rise to systemic level; shunt flow right-to-left
Pregnancy complications: at term and during 1st postpartum week
High frequency of: spontaneous abortion, IUGR, preterm labor
Maternal mortality rate: primary pulmonary hypertention ~ 30%; Eisenmenger syndrome ~36%; secondary vascular pulmonary hypertention ~56%
Perinatal mortality due mainly to prematurity
Neonatal mortality rate: 12%
Preconception counseling: extreme risk from pregnancy; pregnancy is contraindicated!
Acquired heart disease - Mitral stenosis
The most common valvular lesion in pregnancy Hypervolemia and tachycardia exacerbate
transmitral gradient Symptoms: asymtomatic, dyspnoea, cough
Even asymptomatic patients (mild to moderate stenosis) can develope atrial fibrillation and heart failure in antepartum/peripartum period! Pulmonary oedema.
Outcomes
No maternal mortality
Morbidity (heart failure and arrhytmias)
Risk of complications higher in patients with a history of cardiac events: arrhytmias, stroke, pulmonary oedema
Fetal/neonatal outcomes: risk increases with severity of mitral stenosis
Management
In patients in NYHA class III or IV (despite optimal medical therapy), percutaneous mitral valvuloplasty during pregnancy should be considered
Other rheumatic lesions
Rheumatic aortic stenosis: risk similar to congenital aortic stenosis
Aortic or mitral regurgitation – well tolerated during pregnancy
Function may deteriorate (NYHA classification)
Peripartum cardiomyopathy
Idiopathic dilated cardiomyopathy, involves ventricular systolic dysfunction that developes during the last month of pregnancy or in the first 5 months after delivery in patients with no known underlying disease
Heart failure – the most common manifestation; others: arrhytmias, embolic events
Outcomes: improvement in NYHA functional status postpartum or persisting/worsening heart lesion
Relapse rate in subsequent pregnancy:- Substantial in women with persisting cardiac
enlargement / left ventricular dysfunction- Possibility of persistent subclinical
dysfunction (despite of recovered systolic function)
Atheromatous coronary artery disease
If possible – assessment (exercise testing) and treatment (coronary bypass surgery) before pregnancy
Risk in pregnancy: angina developement, myocardial infarction, especially in the peripartum period
Coronary angiography: recognition of mechanism of the infarct
Management
Thrombolytics shoul be avoided if coronary artery dissection occured
Percutaneous intervention (PCI) with stenting is optimal
Differentiate with: congenital coronary anomalies, disease with aneurysm formation, coronary arteriitis, autoimmune vascular diseases
Clinical approach - general recommendations:
1. Risk stratification
2. Antepartum management
3. Peripartum management
4. Recurrence of congenital lesion in the
neonate
5. Site of antepartum and peripartum care
Risk assessment
Cardiovascular history and examination 12-lead electrocardiogram Transthoracic electrocardiogram Arterial oxygen saturation measurement by
percutaneous oximetry in cyanotic patients Define underlying cardiac lesion Assess: ventricular function, pulmonary pressure,
severity of obstructive lesions, persistence of shunts, hypoxemia
Low risk
Small left-to-right shunt Repaired lesions without residual cardiac
dysfunction Isolated mitral valve prolapse without significant
regurgitation Bicuspid aortic valve without stenosis Mild/moderate pulmonic stenosis Valvular regurgitation with normal ventricular
systolic function Patient can be managed in a community hospital
High risk
Significant pulmonary hypertention Marfan syndrome with aortic root or major
valvular involvement Peripartum cardiomyopathy with residual left
ventricular systolic dysfunction
Patient should be managed in a high-risk pregnancy unit by a multidisciplinary team staffed by obstetricians, cardiologists, anesthesiologists and pediatricians
Antepartum management
Limiting activity in severely affected patients; hospital admission by mid-second trimester
Pregnancy complications: early identification, aggresive treatment (ie. PIH, hyperthyroidism, infections, anemia)
Mitral stenosis: rather beta-blockers than digoxin Coarctation, Marfan syndrome, ascending
aortopathy: empiric therapy with beta-blockers
Arrhytmias: if possible, avoid drugs in the 1st trimester, but:
Drugs administration for patients with severe symptoms or poor tolerance of sustained arrhytmias
Antiarrhytmic drugs:
preferred: digoxin, cardio-selective beta-blockers, adenosine;
limited use: quinidine, sotalol, lidocaine, flecainide, propafenone;
contraindicated: amiodarone Electrical cardioversion is save Implantable cardioverter-defibrillator
Anticoagulation therapy
Oral warfarin: non teratogenic in dose <5mg per day; risk of fetal intracranial bleeding throughout pregnancy, especially during vaginal delivery unless warfarin stopped before labor
Heparin: less effective in patients with prosthetic valves, safe for the fetus 6-12 Hbd
Low-molecular-weight heparin: more stable anticoagulation level
Low-dose aspirin in women with prosthetic valves as a part of antithrobotic regimen
Peripartum management
Elective cesarean section - indicated for: aortic dissection, Marfan syndrome with dilated aortic root, taking warfarin within 2 weeks of labour
Preterm planned induction: in high-risk patients to ensure that appropriate staff and equipment are avaliable; uncommon
Hemodynamic monitoring: no consensus on using invasive procedures during labor and delivery
Replace anticoagulants by heparine at 36 Hbd Give up heparin at least 12 hours before induction Routine antibiotic prophylaxis for endocarditis:
controversial in cesarean section or uncomplicated vaginal delivery; indicated in patients with prosthetic valves or previous endocarditis
Pain control: epidural anaesthesia and adequate volume preloading is recommended
Positioning the patient on her left side lessens hemodynamic fluctuations associated with contractions
Forceps or vacuum extractor at the end of second stage to shorten delivery
Postpartum monitoring of patients at intermediate or high risk: for at least 72 hours
Risk of congenital heart disease in offspring
0.4 - 1% in general population
10 - fold increase if a first-degree relative is affected
Patients of reproductive age with congenital heart disease should be offered genetic assessment and counseling: estimation of transmission risk and information of the options for prenatal diagnosis