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.

Tricuspid Pulmonic Pulmonary capillaries Mitral LV dilation / hypertrophy Aortic stenosis

Aortic stenosis at rest

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

Resistance arterioles

Tricuspid Pulmonary capillaries (edema) LV failure / ischemia 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  shunt  increased SVR  ?RV failure?

increased L  R • 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

ml 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.html

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 aorta.

 L shunt and accidental ligation of the • 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 tchin.org/portraits/angela-1.htm

www.rjmatthewsmd.com/Definitions/po p/23jfig.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  infarction.

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.

LA RA LV RV Ao PA High SVR, Minimal R  L shunt 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 RA LV RV Ao PA Decreased SVR  desaturation 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).

usually increases. CO can increase because volume status is inc in HR and CO, oxytocin bolus with decrease

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