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

• 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

• Patient may need interventional procedure
(valvuloplasty) or termination of
Pulmonary LV dilation / hypertrophy

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
Tricuspid Aortic

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
Repaired Congenital
Heart Disease Patients with no sx.

SBE prophylaxis (amp/gent, vanco/gent)

?1% incidence of CHD in infant alert

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.
Coarctation of aorta
• Uncorrected, is a very
dangerous lesion in

• Increased afterload
for heart, decreased
perfusion for uterus.

• Risks: LV failure,
aortic rupture,

• More common in
Dilated collaterals in coarctation
Descending thoracic aortic coarctation repaired with stent
Tetralogy of Fallot
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.
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
• Hoarseness can be d/t
damage to recurrent laryngeal
nerve at aortic arch.
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
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
Eisenmenger’s syndrome with
pulmonary artery hypertrophy.
Patient is thin, cyanotic and may
have clubbing.
Pulmonary Hypertension (PH)
• What’s the difference from Eisenmenger’s

• 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

• Normally, PA pressure stays the same despite
increased CO.
Passive Influences on PVR:
Capillary Recruitment and Distension

Pulmonic Mitral

Normal circulation at rest.
Cardiac output is limited by SVR.
Heart gives body tissues what they “ask

Resistance arterioles
Pulmonary vascular
resistance falls

Pulmonic Mitral

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

Resistance arterioles– decreased SVR
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

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 arterioles—decreased SVR
How does pulmonary hypertension
kill patients?

• By causing the interventricular septum to
bow into the LV cavity, diminishing its

• 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
• 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, Eisenmenger’s, 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
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 =

– Endothelin antagonist: Bosentan (Tracleer)

– Oral sildenafil (Viagra).
PH and Esiensmenger’s
• High alveolar PAO2.

• Avoid: pain, hypercarbia, hypothermia,

• 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
• 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.

RL shunt

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.

RA RV Increased

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 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; 108:802–11 Copyright © 2008, the
American Society of Anesthesiologists, Inc. Lippincott
Williams & Wilkins, Inc.
Hemodynamic Changes Associated with Spinal
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,
What raises pulmonary vascular

• 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
• Over time LR shunt can lead to
Eisenmenger’s syndrome