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
capillaries

LV dilation / hypertrophy

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
capillaries
(edema)

LV failure /
ischemia

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
tml

www.med.yale.edu/.../cardio/chd/e_a
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 LV
compression

Minimal RV
distention

High pulmonary resistance at rest

Slight bowing of IV septum into LV
cavity.

Resistance arterioles

RV distention
and failure

LV cavity compressed
(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 cardiopulmonary 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

RA

LV

RV

Ao
PA

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

High SVR,
Minimal
RL shunt

Low
pulmonary
vascular
resistance

Decompensated patient with REAL RL shunt.

LA

RA

LV

RV

Decreased
SVR
desaturation

Ao
PA

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).

Bolus CS.
oxytocin Epidural
(10 U in this example)
dramatically lowers
SVR and CO
Repeat
anesthesia.
Delivery
with
usually increases. CO can increase because volume status is adequate,
inc inaortocaval
HR and
CO, has
oxytocin
bolus
withby decrease
compression
been relieved,
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