You are on page 1of 40

CARDIOVASCULAR

DISEASES IN PREG
Dr S.N. Cookey
Consultant Physician Cardiologist
RSUTH
 Pregnancy is a “stress test for life”
 Unveils problems that will appear later.
Such a pity men don’t get this privilege.
Cardiovascular diseases in preg
 Heart diseases complicates 1%- 3% of pregnancies.
 10% –15% of maternal mortality
 Incidence of CVD in preg is on the increase
 70 -80% in the western world is from Congenital Heart
Disease (CHD).
 Subsaharan Africa majority is from rheumatic (VHD)
 Due to migration 15% RHD
 Mortality is less than 3% from RHD in western world.
 While from subsaharan africa 15 preg related deaths
occurred out of 32 women studied.
 Peripartum cardiomyopathy is a consequence of preg.
CARDIOVASCULAR CHANGES IN
PREGNANCY
 Plasma volume
 Cardiac output
 Blood Pressure
 Heart Rate
 ECG
 ECHO changes
PLASMA VOLUME
 Increases significantly in preg.(25 %-100%)
Av. 50%
 Estrogen stimulation of the RAAS

 Prolactin

 Placenta lactogen growth hormone

 Adrenocorticotrophic hormone

 Prostaglandins.

 Results in dilutional anaemia(physiologic

anaemia in preg)
PLASMA VOLUME

 Pl. volume start ↑ by 6 wks

 50% ↑ 2nd trimester then


plateaus till delivery

 Red cell mass ↑ to lesser


extent
CARDIAC OUTPUT

 There is approximately a 50% increase in cardiac


out-put in pregnancy,this starts early in
pregnancy peaks at mid trimester.
 Varies with body position increasing in the lateral
position and reducing in the supine position
 Uterocaval syndrome
 Early rise is from augmented stroke volume
 Late rise is attributed to increased heart rate.
 Pregnancy with multiple fetuses is associated
with HR
Heart rate & Stroke Volume
Heart rate
 ↑ 10 – 20 %
 remains high 2–5 d after
delivery

SV
 ↑ from 8 wks
 Peak at 20 wks
 ↓ to baseline by 2 wks PP
CO Distribution
CO Variation with position
CARDIAC OUTPUT
 Beginning of labor : > 7 L/min
 Uterine contraction : > 9 L/Min
 Anesthesia : < 8 L/min

 CO falls to non pregnant values in few wks


after delivery

 CO ↑ in twins or triplets is only slightly greater


than in single pregnancy
BLOOD PRESSURE
 There is a fall in blood pressure during early
trimester but it begins to rise and in third
trimester returns to the pre pregnancy value.
 Drop in BP is from reduced peripheral vascular
resistance due to gestational hormones, ANP,
NO,PG
 Supine hypotension syndrome of pregnancy
BP & SVR
Haemodynamic changes in labour,
delivery and postpartum
 Naturally haemodynamically
decompensating.
 Pain
 Anxiety
 Maternal position
 Blood loss(500mls SVD, 1000mlsC/S)
 Uterine contraction(10-20mmHg rise)
 Analgesia blunts haemodynami alteration
 Valsalva maneuvre
Hemodynamic changes in pregnancy, labor and postpartum.

Michael Nanna, and Kathleen Stergiopoulos J Am Heart


Assoc 2014;3:e000712

© 2014 Michael Nanna, and Kath


Clinical FindingsElevated
in Normal Pregnancy
JVP [↑plasma vol]

S1 Loud
↓B.S. at lung bases S2 wide split , accentuated [P2 delayed]
S3
Flow murm @ aortic, pulm; ESM
cervical venous hum, mammary souffle

Apex slightly left & up , prominent


impulse

Tachycardia
Pedal oedema : low DBP
↑ plasma vol & PP ↑ [bounding pulses]
venous pressures
ECG

 Tachycardia
 LAD : elev. Diaphragm
 Increased ventricular voltage
ECHO

 Increased LV diastolic dimension


 Increased LV wall thickness
 ↑ LVOT & RVOT velocities
Cardiac Dx
 Congenital
 Valvular
 Cardiomyopathies
 Hypertension
 Arrythmias:
Predictors of Cardiovascular Events
during Pregnancy

 NYHA class III / IV or cyanosis


 Previous cardiovascular event
 Left heart obstruction
 Ejection fraction ≤0.40

 No. of points  % Adverse Events

  0 4-12
1 27-30
>1 62-100
WHO CLASS I RISK
 Uncomplicated, small or mild
PS
PDA
MVP
 Successfully repaired simple lesions
ASD , VSD , PDA ,
Anomalous pulmonary venous drainage.
WHO CLASS II RISK
 Unoperated atrial or ventricular septal defect

 Repaired tetralogy of Fallot

 Most arrhythmias
WHO CLASS III RISK

 Mechanical valve
 Systemic RV
 Fontan circulation
 Cyanotic heart disease (unrepaired)
 Complex congenital heart disease
 Marfan syndrome : Aorta 40 - 45mm
 BAV : Aorta 45 - 50mm
WHO CLASS IV RISK
(pregnancy contraindicated)
 PAH
 Sev. Ventricular dysfunction (LVEF <30%, NYHA
III - IV)
 Sev. MS , sev. symptomatic AS
 Marfan syndrome : Aorta >45 mm
 BAV : Aorta > 50 mm
 Severe coarctation
Timing of Interventions
Percutaneous therapy

 After 4th month in 2nd trimester

 By this time
organogenesis is complete
the fetal thyroid is inactive
Uterus size small
Mode of delivery

 Depends on the haemodynamic status of the patient and obstetric


indications(multidisciplinary approach)(Obst, Anaes,Cardiologist)
 Tertiary hospital
 Preferred mode : vaginal

 Caesarean delivery : obstetric indications

 Caesarean delivery considered for pts


On oral anticoagulants
Marfan syndrome aorta > 45 mm
Aortic dissection
Intractable heart failure
Eisenmenger syndrome
 Also in sev. AS , pts with mechanical prosthesis
LABOUR

 Lumbar epidural analgesia


↓ pain related sympathetic activity

 Lateral decubitus position

 ↓ 2nd stage : forceps or vacuum extraction


HEART FAILURE MDICATIONS IN
PREG
 FUROSEMIDE
 DIGOXIN
 HYDRALAZINE
 ALDOSTERONE ANTAGONIST (aldactone
and epleronone)
 NITRATES
 BETA BLOCKERS
 Pre conception counseling
RHDX
 Good history and clinical findings for assessment of severity and
information on prosthetic valve
 Electrocardiogram for heart rhythmn
 C-xray for pulmonary congestion
 Comprehensive transthoracic echocardiogram with 2D and
Doppler interrogation( direct planimetry for MVA in preg)
 TEE for assessment of treatment options
 Computed Tomography (CT)
 Cardiac resonance imaging (MRI)
 Stress Testing
 Cardiac catheterization
 Surgical risk evaluation
 Follow-up
RHDX
 Severity
Presence or absence of symptoms
Severity of VHD
Right or left ventricular response to volume or
pressure overload.
Effect on pulmonary or systemic circulation
Change in heart rythmn
For stenotic leison very severe stenosis
(TTE gold standard and recommended class 1A)
Algorithm of preconception counseling and evaluation. *A heart valve team includes
monitoring in a tertiary care center with a dedicated a team of cardiologists, surgeons,
anesthesiologists, and obstetricians with expertise in the management of hi...

Michael Nanna, and Kathleen Stergiopoulos J Am Heart


Assoc 2014;3:e000712 © 2014 Michael Nanna, and Kath
TREATMENT
 Treatment of a specific valvular lesion during
pregnancy may be required in the presence of
heart failure, arrhythmia, or hemodynamic
deterioration, in order to prevent significant
maternal or fetal morbidity or mortality.
 Therapeutic options for patients with RHDX
include both medical and surgical alternatives,
as well as catheter‐based interventions if
available, with the choice dependent on the
degree of stenosis and patient symptoms.
 Medical therapy includes limitation of activity,
use of diuretics and beta‐blockers for symptom
control if heart failure or atrial arrhythmias are
present.
  Patients with atrial fibrillation, left atrial
thrombus, and/or a history of embolism
should receive therapeutic anticoagulation. 
 Medically refractory pregnant patients with
severe symptoms and/or pulmonary artery
pressure >50 mm Hg may benefit from open
valve replacement surgery when percutaneous
valvuloplasty is not an option
 Fetal compromise remains a major issue with
open surgery.
 Vaginal delivery is preferred
 in patients with mild VHDX, and in patients with
moderate or severe HDX in whom symptoms are
NYHA Class I‐II without pulmonary
hypertension
 Cesarean section may be considered in patients
with moderate or severe dx with Class III‐IV
symptoms, or who have pulmonary hypertension
despite medical therapy, in whom percutaneous
valvuloplasty cannot be performed, or has failed.
Class Recommendation

For women requiring long‐term vitamin K


antagonists who are attempting pregnancy vitamin K antagonists

Preg
LMWH

Pregnant women with mechanical heart valves


•(A) Adjusted‐dose bid LMWH throughout pregnancy.
•(B) Adjusted‐dose UFH throughout pregnancy administered
subcutaneously every 12 hours in doses adjusted to keep the mid ‐interval
•(C) UFH or LMWH (as above) until the 13th week, with substitution by
vitamin K antagonists until close to delivery when UFH or LMWH is
resumed.
In women judged to be at very high risk of
thromboembolism in whom concerns exist about
the efficacy and safety of UFH or LMWH as •), vitamin K antagonists throughout pregnancy with replacement by UFH
dosed above (eg, older generation prosthesis in or LMWH (as above) close to delivery is recommended
the mitral position or history of
thromboembolism
For pregnant women with prosthetic valves at
high risk of thromboembolism, •we suggest the addition of low‐dose aspirin, 75 to 100 mg/day.

•Avoid the use of oral direct thrombin (eg, dabigatran) and anti‐Xa (eg,
rivaroxaban, apixaban) inhibitors

You might also like