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