CVD IN PREGNANCY
PREGNANCY-SPECIFIC CHANGES
- 30-50% increase in the circulating blood volume, resulting from an increase in the volume of plasma
- Decrease in blood viscosity, Relative anemia
- Hypoalbuminemia – lower limb edema
- Retention of sodium and water – enhanced secretion of aldosterone (progesterone, estrogens, placenta)
- Myocardial contractility indices remain unchanged
- 40-50% increase in cardiac output at rest
(beginning at ~6 weeks, peak values at 28-30 weeks)
Results from:
increase in stroke volume, ca. 15% increase in heart rate, ca. 20% increase in oxygen uptake - A 30-50% increase in the circulating blood volume.
1st trimester
decrease in blood pressure, mostly diastolic
decrease in vascular resistance (progesterone)
decrease in pulmonary and peripheral vascular resistance,
increase in vascular compliance
- The last 2 months of pregnancy – a decrease in hemodynamic load
- Delivery – an increase in hemodynamic load
Orthostatic hemodynamic disorders
(changes in cardiac output)
- Supine position – compression of the inferior vena cava
by the gravid uterus – problems with venous return – the so-called supine hypotensive syndrome
decrease in blood pressure, pallor, decrease in heart rate, chest pain, syncope
Change into a lateral recumbent position – resolution of the ailments
SUMMARY
- stroke volume: Normal: 70 /min, Pregnancy: +10-20%
- cardiac output: Normal; 75 ml, Pregnancy: +30%
- blood volume/ Normal 5 L, Pregnancy: +30-50%
- syst. resistance: Normal 1550 N/cm/s, Pregnancy:-20%
- mean pressure: Normal 85 mmHg, Pregnancy: insignificant
- oxygen uptake: Normal: 250 mL/min, Pregnancy +20-30%
pregnancy risk assessment
Older maternal age
History of cardiovascular failure
Higher functional class before and during pregnancy
Atrial fibrillation
CRITICAL PERIODS
24-36 weeks (peak load at 28-34 weeks)
labor and first 2 days postpartum
2-week puerperium
- Congenital defects (atrial septal defect, ventricular septal defect, patent ductus arteriosus, pulmonary stenosis, aortic coarctation, tetralogy of Fallot, Eisenmenger’s syndrome, primary pulmonary hypertension)
- Acquired defects (mitral stenosis, mitral and aortic insufficiency, aortic stenosis, mitral valve prolapse)
- Myocarditis, Arterial hypertension, Cardiomyopathies, Coronary artery disease, Arrhythmia, Status after heart transplant
STAGES OF HEART FAILURE
according to the New York Heart Association (NYHA)
Class I – No limitation of physical activity. Ordinary physical activity does not cause cardiovascular symptoms.
Class II – Slight limitation of physical activity. Ordinary physical activity does not cause cardiovascular symptoms (dyspnea, anginal pain, fatigue, palpitation).
Class III – Less than ordinary physical effort causes cardiovascular symptoms, resulting in limitation of activity.
Patients do not experience the symptoms at rest.
Class IV – The symptoms manifest at any physical activity and are present even at rest.
PREGNANCY-RELATED RISK FOR MATERNAL MORTALITY
- Group I – minimal risk (mortality < 1%)
pulmonary/tricuspid valve disease
biological valve
mitral stenosis (NYHA class I or II) - Group II – moderate risk (mortality 5-15%)
mitral stenosis with atrial fibrillation, artificial valve
mitral stenosis (NYHA class III or IV), aortic stenosis
history of myocardial infarction - Group III – high risk (mortality >25%)
pulmonary hypertension
HEART DEFECTS IN PREGNANCY
labor and puerperium
- increase in heart rate during labor > 110/min.
- respiratory rate > 25/min.
- progressive cyanosis
- Labor is associated with increased risk for infectious endocarditis - 5-7 days of antibiotic prophylaxis
- Hospitalization until cardiovascular stabilization
ACQUIRED HEART DEFECTS
mitral stenosis
Risk assessment
- I NYHA - heart not enlarged, without the signs of congestion, regular sinus rhythm – safe pregnancy and labor
- II NYHA - risk of sudden deterioration
increase pulmonary resistance, increase cardiac output,
increase venous return - II/III NYHA – consider commissurotomy or valvuloplasty
- IV NYHA – pregnancy contraindicated
- Optimally, the defect should be corrected before pregnancy
- Indications to commissurotomy or valvuloplasty in pregnancy:
Absolute: pulmonary edema,persistent pulmonary congestion, hemoptysis.
Scheduled procedure: optimally between 20 and 24 weeks
Emergency procedure – at any time of pregnancy
LABOR
- Maintain heart rate at 70-90/min
Control of pain – spinal anesthesia, narcotics
Avoid terbutaline
Beta-adrenolytics in tachycardia
Reduce activity
- Maintain preload:
Avoid heavy blood loss
Avoid overhydration - diuretics
I NYHA – V.D.; II-III NYHA C.S.
- Normal area of the mitral valve orifice – 4.0-5.0 cm2
- Mitral valve orifice area <1.5 cm2
significant limitation of left ventricular filling at diastole
preventing appropriate increase in cardiac output
decrease in left ventricular preload - tachycardia,
increase in left atrial preload - arrhythmia - atrial fibrillation – pulmonary edema (usually at 28-32 weeks)
aortic stenosis
- Rarely as an isolated cardiac defect
- Results from developmental malformation of the valves
(especially tricuspid valve) or has rheumatic origin - (+) circulating blood volume - (+) left ventricular pressure - (+) valve gradient - (+) left ventricular load
- Women >30 years of age and pre-pregnancy NYHA class II may present with anginal pain, syncope, acute left ventricular heart failure and sudden death due to arrhythmia
- Young women – pregnancy well tolerated by limited exercise (valve gradient <50 mmHg)
aortic insufficiency
- Maternal risk is determined by severity of the defect
- Women with asymptomatic insufficiency - pregnancy well tolerated
- (-) peripheral resistance, shortened diastolic time, (-) mitral regurgitation (relative)
- Severe aortic insufficiency: markedly enlarged heart, electrocardiographic signs of left ventricular overload: pregnancy – rapid circulatory failure
LABOR
SEVERE
- Area <1 cm2, Gradient >75 mmHg, EF <55%
- Surgical correction
MODERATE
- Area <1-1.5 cm2, Gradient 50-75mmHg
- Limited physical activity, Monitoring of symptoms
MILD
- Area >1.5 cm2, Gradient <50 mmHg
- Limited physical activity, Monitoring of symptoms
mitral valve prolapse
- Most common heart defect in young women (30% of population)
- Usually asymptomatic (palpitations - beta-adrenolytics)
- Incidence of pre- and postpartum complications - similar as in general population
- Pregnancy and labor well tolerated
peripartum cardiomyopathy
DIAGNOSTIC CRITERIA
Classic
- development of heart failure during the last month of pregnancy or within 5 months after birth
- lack of established cause of heart failure
- lack of diagnosed heart disease before the last month of pregnancy
Additional (ultrasonography)
EF < 45%
Shortening fraction < 30%
End-diastolic left ventricular diameter >2.7cm/m2 body area
RISK FACTORS
- multiparity, older maternal age, multiple pregnancy
- preeclampsia, arterial hypertension
MYOCARDIAL INFARCTION
Risk factors
- tobacco smoking, arterial hypertension, obesity
- older age, hyperlipidemia, diabetes mellitus
- Mode of labor is determined by clinical manifestation:
cesarean section (coronary instability)
shorter 2nd phase of labor, spinal anesthesia - Oxytocin and Metergin are not recommended due to potential risk of coronary artery constriction
etiology
- atherosclerosis, primary or secondary vasospasm (medications, preeclampsia)
- thrombangiitis obliterans, congenital defects (abnormal ramifications of coronary arteries)
- hypertrophic cardiomyopathy, spontaneous coronary artery dissection
ROUTINE TREATMENT
- ROUTINE: (beta-adrenolytics, aspirin, calcium channel blockers, nitrates, thrombolytic therapy)
- Lack of improvement: INVASIVE TREATMENT: coronarography, PTCA, by-pass
Risk: arrhythmia, arterial embolism, toxicity of a contrast agent, vascular injury
LABOR
- In patients requiring cardiac surgery, cesarean section should be considered after the 28th week, i.e. prior to the surgical treatment
- Coronary instability in early pregnancy constitutes indication to termination
- Whenever possible, labor should be avoided up to 14 days after the fresh myocardial infarction
- Decision on the mode of pregnancy termination after myocardial infarction should be based on usual obstetrical indications and clinical status of a mother
Supraventricular arrhythmia
- isolated supraventricular premature beats - relaxation, Isoptin, selective beta-blocker, digitalis
- paroxysmal tachycardia: usually nodal (reentrant)
sedation, Valsalva maneuver, carotid sinus massage, Isoptin 5-10 mg i.v., selective beta-blocker,1st and 2nd trimester - adenosine.
- paroxysmal atrial fibrillation - poorly tolerated by a patient – electric cardioversion
- asymptomatic atrial fibrillation – pharmacological cardioversion (propafenone, procainamide, chinidine)
- chronic atrial fibrillation - digoxin, anticoagulation therapy
HEART DEFECT
LABOR
- prophylactic antibiotic therapy:
artificial valve, history of a rheumatic disorder,
acquired or congenital cardiac defect
history of infectious endocarditis
hypertrophic cardiomyopathy
mitral valve prolapse and regurgitation after cardiac surgeries
anticoagulation therapy
- 1st trimester - heparin (2-2.5-fold increase in APTT)
- 2nd trimester - coumarin derivatives (INR 2.0 – 3.0)
- 3rd trimester - heparin (2-2.5-fold increase in APTT)
- Intrapartum - withdrawal of heparin
- Postpartum- reimplementation of heparin at 6-12 h
coumarin 3-6 days after labor
management
- Reduction of physical exercise level
- 1st trimester – pharmacotherapy only if absolutely necessary (developmental defects – impaired organogenesis)
- 2nd trimester – rest in a lateral recumbent position
- Hospitalization - beginning at peak hemodynamic load
- Avoidance of standing position
- Dietary restriction of salt and fluids