Aortic Stenosis in Pregnancy

Brendan Astley MD
&
Norman Bolden MD
Nov 2006

18 year old G1P0 Spanish

speaking female
PMH- Heart condition since age 12 (no further
follow-up)
SOB and CP at rest and exertion worse over last
two years
PSH- none
Medications- PNV
Allergies- NKDA
FH- unknown
SH- no tobacco, EtOH or drug use

Physical Exam
Vitals BP 104/62 HR 79 temp 36.6 RR 18
sat 100%
Height 410 Weight 99lbs. now 119lbs.
Heart IV/VI systolic murmur cresendo-decresendo
murmur with no diastolic component, heard best at R
upper sternal border, radiation to carotids bilaterally, no
JVD, no 3rd or 4th heart sound
Airway nml, Mal I
Lungs CTA Bil., no w/r/r
Abd NT gravid uterus, soft
Ext no edema good pulses distally

Labs: B positive
BNP 5.5
WBC 8.71, Hg 12.5, Hct
36.8, Plts 256
Na 136, K 3.9, Cl 108,
CO2 21, BUN 5, Cr 0.5,
Glu 71
Ca 8.5
TSH 0.9, RPR, NR, HIV,
VZ immune, RI, GC/
chlam, hep B all negative

Plan: Admit to antepartum

unit (social admission) to
facilitate consultations by
Maternal/Fetal Medicine,
Cardiology, NICU and
Anesthesiology.

Cardiology
Murmur appreciated and echo performed: on
9/15 showing AS <.6cm2, probable bicuspid
valve and EF 65%.
Pt followed for change in symptoms.
Mid Oct. at about 35 wks. Gestation she
complains of increased CP and SOB especially
with exertion but also at rest.
.1%-1.4% pregnancies with clinically significant
cardiac problems
Mortality from these .5%-2.7%

Cardio contd
Echo shows peak gradient of 62mmHg
and .58cm2 orifice by the continuity
equation.
Velocity waveform is asymmetric which
usually equates with less than severe
stenosis.
CXR- WNL, no cardiopulmonary disease
CXR abnormalities may include enlarged
aorta, cardiomyopathy and possibly pulm.
edema

Expected EKG changes with AS

Left ventricular hypertrophy (LVH)
There are many different criteria for LVH.
Sokolow + Lyon (Am Heart J, 1949;37:161)
S V1+ R V5 or V6 > 35 mm

Cornell criteria (Circulation, 1987;3: 565-72)

SV3 + R avl > 28 mm in men
SV3 + R avl > 20 mm in women

Framingham criteria (Circulation,1990; 81:815-820)

R avl > 11mm, R V4-6 > 25mm

S V1-3 > 25 mm, S V1 or V2 +
R V5 or V6 > 35 mm, R I + S III > 25 mm

Romhilt + Estes (Am Heart J, 1986:75:752-58)

Point score system

Left atrial abnormality (dilatation or hypertrophy)

M shaped P wave in lead II
prominent terminal negative component to P wave in lead V1

? Suggestions for Anesthetic Plan

Anesthesia for Vaginal Delivery
Monitors for Vaginal delivery
Anesthesia for C/S
Monitors for C/S.
Maternal-Fetal Medicine, Cardiology , NICU, and
Anesthesia develop working plan.
***If possible, avoid C/S. If vaginal delivery,
must avoid valsalva.

Anesthesia for Vaginal Delivery

Neuroaxial anesthesia
Continuous Spinal
Single shot spinal not reasonable for prolonged labor
Reliable block
Intrathecal narcotics avoid the sympathectic block with
ensuing hypotension
Intrathecal narcotics not effective for second stage of labor.
Small doses of intrathecal LAs added to narcotics improve
analgesia while limiting hemodynamic consequences.
Chance for spinal headache

Anesthesia for Vaginal Delivery

Neuroaxial anesthesia
Epidural
Prostitratable to produce minimal hemodynamic
changes, adequate anesthesia possible for vaginal
or C-section, if performed properly no spinal
headaches
Conshigher failure rate compared with spinal

Anesthesia for Vaginal Delivery

IV Narcotic analgesia (PCA)
Proswould offer patient some analgesia
(most still report 8-10/10 pain despite
Fentanyl PCA)
Cons Respiratory Depression (mother and
fetus), Sedation (mother and fetus), N/V,
decreased beat to beat variability on fetal
heart rate tracing.
Cons.Would not effectively control the pain
from second stage of labor and therefore
would not attenuate the increase in HR
associated with delivery.

Stages of Labor
1st stage 2 phases:
latent phase encompasses the onset of pain
to the first noticed change in cervical dilation
Maximal dilation phasebegins around 3 cm

2nd stage Maximal cervical dilation 10cm

until delivery of fetus
3rd stage After delivery of fetus until
delivery of placenta

Board Questions??
During the first stage of labor, the pain of
uterine contractions is transmitted via
spinal cord segments..
AT6 to L1
BT6 to L5
CT10 to L1
DT10 to S1
ET10 to S5

Answer is.C

Anesthesia for C-section

General anesthesia
Prosgood airway control, minimal hemodynamic
changes compared to epidural/spinal boluses to start
case, can treat hemodynamic changes rapidly with
close monitoring
Conspossible difficult airway, aspiration risks,
tachycardia and/or hypertension on induction or
emergence, caution with volatile agents and
hypotension or myocardial depression

Hospital Course
Induced to L & D at 35 weeks.
Arterial line placed
Swan-Ganz catheter placed
Early epidural also placed by anesthesia
Continuous Telemetry monitoring
Pitocin was started on the night of 11/7
and by morning she was well dilated and
contracting regularly

PCWP/CVP readings
11/7
1950hrs: PCWP 10-11, CVP 5-7, good UOP
2330hr: PCWP 10-13
11/8
0100: PCWP 7-9complains of CP
0300:CVP 15-16, trop .15
0500: PCWP 11-15, CO 5L/min
0800: trop <.1 (nml)
Wedge maintained in above normal range
Delivery at 1130am

Hospital Course contd

No symptoms of AS during induction
course.
Ready for delivery in AM with forceps
No valsalva by mother and epidural
working well with slow dosing.
PCWP and urine output maintained
throughout delivery with fluids and gentle
epidural dosing.

Hospital Course contd

After forceps delivery pt transferred to StepDown on esmolol drip due tachycardia.
Drip stopped in CCU 11/8 and gentle diuresis
started with Lasix.
Stable vital signs throughout hospital stay.
Day #3 post-forceps delivery patient transferred
home with 6 week follow-up with cardiology for
possible valve replacement.

Physiologic Changes during

pregnancy
Beginning to change at 5 weeks10 fold
increase in uterine blood flow at term
Cardiovascular : Blood volume 35%, CO
40-50%, SV 30%, HR 15-20%
Cardiovascular : SVR 15%, sys and diastolic
BP 10mmHg
Pulmonary Changes: O2 consumption 20%,
RR 15%, MV 50%, TV 40%, alv vent. 70%
ERV 20%, FRC 20%

Aortic Stenosis
In the past Rheumatic Valvular degeneration
was the primary cause
Congenitally bicuspid valves become calcified
and cause stenosis most commonly now(1-2%
of population)
Senile degeneration can also occur
30% of patients older than 85 have significant
changes
Risk for sudden death with AS increases when
grad. >50mmHg and orifice less than .8cm 2

Normal Anatomy

Aortic stenosis Anatomy

AS 2D echo

Symptoms
Rheumatic AS patients may remain
asymptomatic for 40 years
Bicuspid valve patients will develop
symptoms between 15-65 years of age
Calcifications of the valve usually occur
after age 30
THE TRIAD.

The triad
Any one of these symptoms being present
is ominous and the patients life
expectancy is less than 5 years
ANGINA
SYNCOPE
CHF

Angina
This is the initial symptom in 50-70% of
patients. Most commonly occurring with
exertion
May be present without CAD b/c of
Increased myocardial O2 consumption, with
increased myocardial thickness and increased
afterload
Also increased LVEDP impairing flow to
subendocardial layers

Syncope
First symptom in 15-30% of patients
Once this occurs the average life
expectancy is 3-4 years
Origin of syncope is controversial,
however it may be related to
uncompensated decrease in SVR with
exercise

CHF
Due to diastolic dysfunction (increased LV
thickness) or systolic dysfunction (increased
afterload or decreased myocardial contractility)
Once LV failure occurs the average life
expectancy is 1-2 years
All AS patients are at increased risk of sudden
death, as previously stated and.
Only 18% of patients are alive 5 years after the
peak systolic gradient is >50mmHg or the orifice
<0.7cm2

Pathophysiology
Stage 1: asymptomaticmild stenosis
Normal stroke volume maintained as gradient
between LV and aorta increases
Higher gradient results in concentric LV
hypertrophy

Pathophysiology
Stage 2: moderate stenosissymptomatic
Dilation as well as hypertrophy occur in this
stage
Decreased EF may be noted (due to
decreased contractility)
Increased LVEDP and LVEDV leads to
increased myocardial work and O2
consumption.at risk myocardium

Pathophysiology
Stage 3: critical AS
Valve area is less than .5cm2/m2 and EF
decreases further with further increases in
LVEDP
Pulmonary edema when LA >25-30 mmHg
RV failure will develop if sudden death does
not occur first

Calculation of Stenosis
Gorlin equation: AV area (cm2)=
CO (L/min)/
Mean pressure gradient1/2
This is the simplified version of the Gorlin
equation (Hakki equation)

Continuity equations
AV area=LVOT velocity/AV velocity x LVOT area
---LVOT calculation can have errors because its
an area squared.
AV area= CO/(HR x systolic ejection period x
44.3 x gradient in mmHG1/2) ---Gorlin equation
weak under low CO states
Hakki equationbased on the fact that HR x sys
ejection period x 44.3= 1000; therefore AV Area=
CO/ sq root of gradient (mmHg)

PA Cath
Because of increased LVEDP stretching
the mitral annulus a prominent v wave can
be observed with disease progression. LA
hypertrophy develops and the A wave
becomes prominent
Example to follow on next slide

Arterial line
Pulsus parvus (narrow pulse pressure)
Pulsus tardus (delayed upstroke)
These features make the wave appear
overdampened

Hemodynamic profile
AS increase LV preload and SVR
Decrease HR
Keep contractile force and PVR constant

Preload because of Decreased LV

compliance as well as Increased LVEDP
preload augmentation is needed
(caution with nitro)

Hemodynamics continued
Heart rate no extremes of HR
Increase HR = decreased coronary perfusion
Sinus rhythm important for added EF

Contractility
avoid B-blockers they can increase LVEDP
and decrease CO

Hemodynamics continued
SVR most of afterload is due to stenotic
lesion, therefore its fixed.
If SBP is decreased the patient can develop
subendocardial ischemia
Early alpha-adrengic agonists needed as
treatment

PVR this stays normal until very late in

the disease process

Toronto study
1986-2000 of 49 pregnancies in women
with AS
Mild AS (>1.5cm2 or grad<36mmHg)
Mod AS (1.0-1.5cm2 or grad 36-63mmHg)
Severe AS (<1.0cm2 or grad >63mmHg)

All women had functional NYHA class I or

II disease when enrolled
59% of patients, 29/49 had severe AS
Silversides C.K., Colman J.M., Sermer M., Farine D., Sui S. C., Early and intermediate-term outcomes of pregnancy with congential aortic
stenosis. American Journal of Cardiology 2003;91:11

NYHA functional classification

Class I Asymptomatic
Class II Symptoms with greater than
normal activity
Class III Symptoms with normal activity
Class IV Symptoms at rest

Toronto study continued

10% of severe AS patients (3/29) had early cardiac
complications (pulmonary edema or atrial arrhythmias)
no complications in mild/mod groups
One pt. had AVA .5cm2, peak gradient 112mmHg, she
developed pulmonary edema at 12 weeks had emergent
aortic valvuloplasty then had a Ross procedure 4 years
after delivery
The second pt. had gradient of 104mmHg; she had
postpartum hemorrhage, hypotension and subsequent
pulmonary edema. Resection of her subaortic membrane
was performed 17 months after delivery.
The third pt had a bicuspid valve AVA .7cm2, gradient of
64mmHg, she had atrial arrhythmias during antepartum
period. She underwent a Ross procedure 18 months
postpartum.

Toronto Study continued

8% mild/mod AS had cardiac surgery in followup and 41% of severe AS group had postpartum cardiac surgery10% with severe AS
had cardiac complications during pregnancy
12 pregnancies complicated by preterm birth,
resp. distress syndrome, IUGR
Rate is similar general population

No fetal or neonatal deaths

Silversides CK, Colman JM, Sermer M, Farine D, Siu SC. Early and intermediate-term outcomes
of pregnancy with congenital aortic stenosis. Am J Cardiol 2003;91(11):1386-9

Brazilian study
Study of 1000 women with heart disease
followed between 1989-1999
HD-- Rheumatic HD 55.7%, Congenital HD
19.1%, Chagas disease 8.5%, arrhythmias
5.1% and cardiomyopathies 4.3%
A subset of patients who had moderate to
severe AS experienced 68.5% maternal
morbidityi.e. CHF & angina
2 needed Aortic valve replacement
1 sudden death
Avila WS, Rossi EG, Ramires JA, Grinberg M, Bortolotto MR, Zugaib M, et al.
Pregnancy in patients with heart disease:experience with 1000 cases. Clin Cardiol
2003;26(3):135-42

Anesthetic management goals

Maintain Normal Sinus Rhythm: up to 20%
of CO is provided by atrial kick in a normal
patient and possibly up to 40% in AS pts.
Maintain HR 70-90: Bradycardia
decreases CO in pt with fixed stenotic
lesion and tachycardia does not allow for
diastolic filling of ventricles.
Generous preload: maintain at normal to
high range.

Anes. Management goals contd

Close hemodynamic monitoring: Arterial line and
with moderate to severe stenosis- PA cath/TEE
to help delineate hypovolemia from CHF. Be
prepared for cardioversion urgently
Lidco may be useful

No Valsalva and minimize pain. These could

affect preload and sympathetic response (HR,
BP) and worsen her condition acutely.
Narcotic based anesthetic preferred in unstable
or severe AS patients (50-100mcg/kg IV)

After Hospital stay

Pt seen by cardiology follow up post-op
and Cardiothoracic surgery
She was recommended for valve surgery
Cardiology has sent her letters warning of
sudden death as this patient has no longer
been coming to her appointments and is
currently lost to follow upwith no valve
replacement