Cardiovascular disease

in obstetrics

Tom Archer, MD, MBA

UCSD Anesthesia
 Heart Disease in Pregnancy
(Developed World)

• Less post-streptococcal rheumatic valve

disease (MS, AS).

• More repaired congenital heart disease.

 Maternal Outcome

• Correlates with NYHA functional class.

• How much can the patient do before she

gets symptoms?

• Let’s hear it for the history!

 Risk factors for maternal cardiac
events

• Poor NYHA class

• Cyanosis
• Myocardial dysfunction
• Prior arrhythmia
• Prior heart failure/stroke.

Siu SC Circulation 2001;104;515-521

 CV in pregnancy– Big Picture

• Increase O2 demand Increased CO

• Stable BP with increased CO means

decreased SVR.

• Slight increase in HR
 CV in pregnancy– Big Picture

• Pregnancy will make stenotic lesions more

symptomatic.

• Patient may need interventional procedure

(valvuloplasty) or termination of
pregnancy.
 Pulmonary LV dilation / hypertrophy
capillaries
Tricuspid
Aortic
stenosis

Pulmonic Mitral

Aortic stenosis at rest

Cardiac output not sufficient to cause
critically high LV intracavitary pressure /
LV failure.

Resistance arterioles
 Pulmonary LV failure /
capillaries ischemia
(edema)
Tricuspid Aortic
Stenosis

Pulmonic Mitral

Aortic stenosis with

increased cardiac output /
arteriolar vasodilation:
Decreased SVR Fall in systemic BP and
/ or increase in LV intracavitary pressure
ischemia or LV failure.

Resistance arterioles– decreased SVR

 CV in pregnancy– Big Picture

• AI and MR are often well tolerated in

pregnancy. Decreased SVR helps forward
flow.
 Repaired Congenital
Heart Disease Patients with no sx.

SBE prophylaxis (amp/gent, vanco/gent)

?1% incidence of CHD in infant alert

pediatrics

Otherwise, “good to go”

 Small ASD, VSD or PDA
• No IV bubbles (LR shunt can reverse).
• Epidural LOR with saline, not air
• Pain increased SVR increased LR
shunt ?RV failure?
• Slow onset epidural preferred. Avoid
sudden drop in SVR which could cause
RL shunt and maternal hypoxia.
 Small ASD, VSD or PDA
• Memorize (and avoid) causes of pulmonary
artery vasoconstriction:
– Alveolar hypoxia
– Hypothemia
– Hypercarbia
– Acidosis
– Pain

Increased PA pressure can convert LR

shunt into RL.
30-50% of congenital heart patients
will have an ASD as part of their
disease complex.

home.cc.umanitoba.ca/~soninr/PS.ht
www.med.yale.edu/.../cardio/chd/e_a
ml
sd/index.html
 Coarctation of aorta
• Uncorrected, is a very
dangerous lesion in
pregnancy.

• Increased afterload
for heart, decreased
perfusion for uterus.

• Risks: LV failure,
aortic rupture,
endoaortitis.

• More common in
males.
www.mayoclinic.org/coarctation-
 Dilated collaterals in coarctation

www-clinpharm.medschl.cam.ac.uk/.../index.html
 Descending thoracic aortic coarctation repaired with stent

www.med.yale.edu/.../c_coarct_1815204/index.html
 Tetralogy of Fallot

http://www.nhlbi.nih.gov/health/dci/Diseases/tof/tof_what.html
Marcus JT
Dong SJ. Smith ER. Tyberg JV. Changes in the radius of curvature of the ventricular septum at end diastole during pulmonary
arterial and aortic constrictions in the dog. [Journal Article] Circulation. 86(4):1280-90, 1992 Oct.
 Tetralogy of Fallot
• Patients with corrected TOF should have
periodic echocardiograms.

• Corrected TOF probably “good to go.” May

have conduction abnormalities.

• Uncorrected TOF needs careful

hemodynamic management b/o potential
shunts R > L or L > R.
 Uncorrected
Tetralogy of Fallot
• Two needs:

– Maintain SVR to avoid increasing RL shunt.

– Maintain RV filling pressure to maintain

pulmonary perfusion (LUD and fluid boluses).
 Patent Ductus Arteriosus
• Common in premature babies
with increased pulmonary
vascular resistance.

• Can lead to cyanosis (RL

shunt) or CHF (LR shunt).

• RL shunt will cause

cyanosis in LEs, with higher
SpO2 in R arm.

• Oximeter or arterial line on

feet will pick up RL shunt
and accidental ligation of the
aorta.
• Hoarseness can be d/t
damage to recurrent
laryngeal nerve at aortic arch.
http://health.yahoo.com/media/mayoclinic/images/image_popup/r7_patentd
uctus.jpg
With PDA shunt can be RL or LR,
depending on the pulmonary resistance.

Shunt can be RL after birth, then reverse

to LR as pulmonary resistance falls, then
become RL again as Eisenmenger’s
syndrome develops (long term pulmonary
hypertension).

www.rjmatthewsmd.com/Definitions/pop/22fig.htm
 Eisenmenger’s Syndrome
• Increased pulmonary flow (LR shunt due to
ASD, VSD or PDA) causes hypertrophy of
pulmonary arteries pulmonary hypertension
reversal of shunt to RL with cyanosis.

• Need to correct LR shunt BEFORE it

reverses.

• Need to correct LR shunt despite normal

ABGs.
 Eisenmenger’s syndrome with
pulmonary artery hypertrophy.
Patient is thin, cyanotic and may
have clubbing.

www.radiofreeithaca.net/search/Hippocrates

www.rjmatthewsmd.com/Definitions/po
p/23jfig.htm

tchin.org/portraits/angela-1.htm
 Pulmonary Hypertension (PH)
• What’s the difference from Eisenmenger’s
Syndrome?

• Eisenmenger’s Syndrome has increased

PVR (hypertrophic changes, incresaed
muscularity) plus a RL hole in the heart
(ASD, VSD or PDA).
PH, Eisenmenger’s Syndrome, AS,
MS and Coarctation of Aorta

• Keep SVR up to avoid inc in CO and / or

dec BP

• Keep SVR up to avoid inc RL shunt

 Pulmonary hypertension—

What causes it?

Exactly how does it kill patients?

What is the flow-limiting resistance
in the entire circulation?

• Normally it is NOT the pulmonary

circulation or any of the heart valves.

• Normally it is the systemic resistance

arterioles (<0.1 mm in diameter)
 Pulmonary vascular resistance
in normal lung

• Normally, increased CO causes decreased

Pulmonary Vascular Resistance via
recruitment and distention of pulmonary
capillaries.

• Normally, PA pressure stays the same despite

increased CO.
Passive Influences on PVR:
Capillary Recruitment and Distension

http://www.lib.mcg.edu/edu/eshuphysio/program/section4/4ch4/s4ch4_19.htm
http://www.pathguy.com/lectures/hipbp.gif
 Pulmonary hypertension
• Acute pulmonary thromboembolism
 Pulmonary hypertension
• Chronic pulmonary thromboembolism
 Pulmonary hypertension develops
when pulmonary arteries develop
abnormal resistance

• When pulmonary vessels become high

resistance (fibrosis, muscular hypertrophy)
they can NOT dilate or recruit and PA pressure
rises with increased CO.
How does pulmonary hypertension
kill patients?

• By causing the interventricular septum to

bow into the LV cavity, diminishing its
capacity.

• Cardiac output falls, BP falls, patient dies.

 How do we keep PH from killing
patients?
• Keep Pulmonary Vascular Resistance down.

• Keep Systemic Vascular Resistance up.

• Prevent increases in CO.

• This same logic applies to any stenotic cardiac

lesion, such as AS!
 Pulmonary hypertension

• PA catheter for actual measurement of PA

pressure and titration of pulmonary
vasodilators.
 In MS, HOCM and AS

• Keep HR down

• “Slow and tight” for stenotic CV lesions.

 Pulmonary Hypertension
• Specific drug Rx:

– Inhaled O2

– Inhaled NO

– IV, SQ, inhaled, oral: Epoprostenol = prostacyclin =

Flo-Lan

– Endothelin antagonist: Bosentan (Tracleer)

– Oral sildenafil (Viagra).

 PH and Esiensmenger’s
• High alveolar PAO2.

• Avoid: pain, hypercarbia, hypothermia,

acidosis

• Maintain adequate SVR to avoid need to

inc CO. Use phenylephrine, not ephedrine.
 RL shunts
• Cyanosis not corrected by increased FIO2.
• Watch out for IV bubbles brain or heart
infarction.
• Keep systemic vascular resistance up to
avoid increased RL shunt.
• Avoid infant crying and other things
(alveolar hypoxia, hypothermia, acidosis,
hypercarbia) which increase pulmonary
vascular resistance.
 Compensated patient with POTENTIAL RL shunt.

LA LV High SVR,
Ao
Minimal
RL shunt
PA
RA RV Low
pulmonary
vascular
resistance

Normal, compensated patient with ASD, VSD or PDA-- high SVR and low
pulmonary vascular resistance minimal RL shunt.
 Decompensated patient with REAL RL shunt.

LA LV
Ao Decreased
SVR
desaturation
PA
RA RV Increased
pulmonary
vascular
resistance
desaturation

Decompensated patient with ASD, VSD or PDA-- Decreased SVR or

increased pulmonary vascular resistance  increased RL shunt and
increased arterial desaturation.
 What lowers SVR?
• Exercise
• Spinal or epidural anesthesia.
• Vasodilating anesthetics (sevoflurane,
isoflurane, desflurane)
• Sodium nitroprusside
• Hydralazine
• Oxytocin
• Fever
• Squatting RAISES SVR (Tetralogy of Fallot).
RepeatBolus CS.
oxytocin Epidural anesthesia.
(10 U in this example) Delivery
dramatically lowers SVR and CO with
usually increases. CO can increase because volume status is
inc inadequate,
HR and CO,
aortocaval oxytocin
compression bolus
has been with
relieved, decrease
and oxytocin, by
SVRcontracting
and BP, the uterus, causes autotransfusion.
increase in CO and SV.
Ensemble of hemodynamic
effects of oxytocin in 15
patients at C-section:

Decrease in SVR
Increase in CO:
Anesthesiology 2008; 108:802–11 Copyright © 2008, the
American Society of Anesthesiologists, Inc. Lippincott
Williams & Wilkins, Inc.
Hemodynamic Changes Associated with Spinal
Anesthesia
for Cesarean Delivery in Severe Preeclampsia
Robert A. Dyer, F.C.A. (S.A.),* Jenna L. Piercy, F.C.A.
(S.A.),† Anthony R. Reed, F.R.C.A.,† Carl J. Lombard,
Ph.D.,‡
 What raises pulmonary vascular
resistance?

• Alveolar hypoxia
• Acidosis
• Hypothermia
• Crying
• Pain (catecholamines)
 LR shunts
• Volume overload to LV. Can cause CHF.
• Can manage with reduction in systemic
vascular resistance (vasodilating
anesthetics).
• Over time LR shunt can lead to
Eisenmenger’s syndrome