PREVALENCE

61,3 per 100.000

White 111.6
Hispanic women 34.3
Black101.7
Asian45.0

Journal of the American Heart Association. 2016;5

Baseline characteritic
Khairy P, Ouyang DW, Fernandes SM, Lee-Parritz A, Economy KE and Michael J. Landzberg. Pregnancy
outcomes in women with congenital heart disease. Circulation 2016;113;517-524
 Physiological Changes 1

The first cardiovascular change associated with

pregnancy
Peripheral vasodilation (induced by progesterone) leading
to A decrease in systemic vascular resistance
 Physiological Changes 2

Cardiac output increases

8 weeks : 20%
20-28 weeks :40-50%
Stroke volume increase 80ml/t
ventricular end-diastolic volume
wall muscle mass
contractility
Heart rate increase
10 to 15 beats per minute
 Physiological Changes 3

Labour leads to further increases in cardiac output

In the first stage: 15%
In the second stage: 50%
abdominal pressure plummeted
pain and anxiety : sympathetic stimulation
pulmonary artery pressure increased
blood back into the circulation with each uterine contraction: 300-500
ml
 Physiological Changes 4
After delivery, cardiac output increases again
immediately : 60-80%
sudden interruption of placental circulation
uterine contraction
relief of caval compression
within 1 h: rapid decline to pre-labour values
Puerperium:
uterine contractions
retented Interstitial fluid returned to circulation
return to normal after 2 weeks
 Physiological Changes 5

The greatest change period in systemic blood circulation

and heart burden
32 to 34 weeks
Intrapartum
3 days postpartum
Easily induced heart failure
 Table 1 -- Normal Hemodynamic Changes During Pregnancy

Hemodynamic Change During Change during Change during

Parameter Normal Pregnancy labor and delivery postpartum
Blood volume 40-50% (autodiuresis)

Heart rate 10-15 beats/min

Cardiac output 30-50 % additional 50%

Blood pressure 10 mm Hg

Stroke volume 1st and 2nd (300-500 mL per

trimester; contraction)
3rd trimester
Systemic
vascular
resistance
MECHANISM
 MECHANISM

This may be related to the expansion of plasma volume

and increase in red cell mass that peaks at 28 to 34 weeks
of gestation, as well as the associated increase in cardiac
load.
 TREATMENT

RATE
CONTROL

RHYTHM
CONTROL
 RHYTHM CONTROL

AMIODARON IS NOT SAFE IN PREGNANCY

FLECAINIDE AND SOTALOL
ELECTRICAL CARDIOVERSION
 RATE CONTROL

DIGOXIN
BLOCKER
 ANTICOAGULATION

1 ST TRIMESTER 3RD
LMWH
2 ND TRIMESTER STOP VITK
VITK ANTAGONIST ANTAGONIST 2-4 WEEK
VITK ANTAGONISTTERATOGENIC
BEFORE DELIVERY
 CONCLUSION

Management of AF should be the same as in non-pregnant

women, but requires faster intervention, even in patients with
a normal heart function, and cautious use of medication to
avoid harm to the fetus.
AF is a rare occurrence during pregnancy
increasing number of pregnancies was associated with
subsequent elevations in AF risk.
Repeated exposure to metabolic, physiological, and hormonal
changes during pregnancy may predispose to AF

refference
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