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?

Lets 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 (LR shunt can reverse).
Epidural LOR with saline, not air
Pain increased SVR increased LR
shunt ?RV failure?
Slow onset epidural preferred. Avoid
sudden drop in SVR which could cause
RL 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 LR

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

home.cc.umanitoba.ca/~soninr/PS.h
www.med.yale.edu/.../cardio/chd/e_a
tml
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-aorta/about.htm
 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 RL 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 (RL

shunt) or CHF (LR shunt).

RL shunt will cause

cyanosis in LEs, with higher
SpO2 in R arm.

Oximeter or arterial line on

feet will pick up RL 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 RL or LR,
depending on the pulmonary resistance.

Shunt can be RL after birth, then reverse

to LR as pulmonary resistance falls, then
become RL again as Eisenmengers
syndrome develops (long term pulmonary
hypertension).

www.rjmatthewsmd.com/Definitions/pop/22fig.htm
 Eisenmengers Syndrome
Increased pulmonary flow (LR shunt due to
ASD, VSD or PDA) causes hypertrophy of
pulmonary arteries pulmonary hypertension
reversal of shunt to RL with cyanosis.

Need to correct LR shunt BEFORE it

reverses.

Need to correct LR shunt despite normal

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

www.radiofreeithaca.net/search/Hippocrates

www.rjmatthewsmd.com/Definitions/pop/
23jfig.htm

tchin.org/portraits/angela-1.htm
 Pulmonary Hypertension (PH)
Whats the difference from Eisenmengers
Syndrome?

Eisenmengers Syndrome has increased

PVR (hypertrophic changes, incresaed
muscularity) plus a RL hole in the heart
(ASD, VSD or PDA).
PH, Eisenmengers 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 RL 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
 Pulmonary
vasculature
Tricuspid
Aortic

Pulmonic Mitral

Normal circulation at rest.

Cardiac output is limited by SVR.
Heart gives body tissues what they ask
for.

Resistance arterioles
 Pulmonary vascular
resistance falls
Tricuspid
Aortic

Pulmonic Mitral

Normal circulation during

exercise / arteriolar dilation:
SVR falls, CO increases.
Pulmonary resistance falls.

Resistance arterioles decreased SVR

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.
Minimal RV Minimal LV
distention compression

High pulmonary resistance at rest

Slight bowing of IV septum into LV
cavity.

Resistance arterioles
RV distention LV cavity compressed
and failure (diastole)

Fixed or increased pulmonary

resistance and / or increased CO
RV distention and failure
Intraventricular septal bulging poor LV filling fall
in CO / BP death.

Resistance arteriolesdecreased SVR

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.

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.
 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!
Hemodynamic management of all stenotic cardio-
pulmonary lesions (PH, Eisenmengers, MS,
HOCM, AS, Coarctation)
Keep systemic vascular resistance up and CO down.

Keep R and L sided filling pressures up.

Avoid anemia and vasodilating anesthetic techniques.

In PH, keep PVR as low as possible (avoid hypoxia,

acidosis, hypothermia, consider pulmonary vasodilators)

Pulmonary vasodilators: NO, Flolan (prostacyclin),

sildenafil, bosentan (Tracleer)
 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 Esiensmengers
High alveolar PAO2.

Avoid: pain, hypercarbia, hypothermia,

acidosis

Maintain adequate SVR to avoid need to

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

LA LV High SVR,
Ao
Minimal
RL shunt
PA
RA RV Low
pulmonary
vascular
resistance

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

LA LV
Decreased
Ao
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 RL 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 with
SVR and CO
usually increases. CO can increase because volume status is adequate,
inc inaortocaval
HR and CO, has
compression oxytocin bolus
been relieved, withby decrease
and oxytocin, contracting
the uterus, causes autotransfusion.
SVR and BP, 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; 108:80211 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)
 LR shunts
Volume overload to LV. Can cause CHF.
Can manage with reduction in systemic
vascular resistance (vasodilating
anesthetics).
Over time LR shunt can lead to
Eisenmengers syndrome