1. Cardiovascular disease in obstetrics
Tom Archer, MD, MBA
UCSD Anesthesia

2. Heart Disease in Pregnancy (Developed World)
Less post-streptococcal rheumatic valve disease (MS, AS).
More repaired congenital heart disease.

3. Maternal Outcome Correlates with NYHA functional class.
How much can the patient do before she gets symptoms?
Let’s hear it for the history!

4. Risk factors for maternal cardiac events
Poor NYHA class
Cyanosis
Myocardial dysfunction
Prior arrhythmia
Prior heart failure/stroke.
Siu SC Circulation 2001;104;

5. CV in pregnancy– Big Picture
Increase O2 demand Increased CO
Stable BP with increased CO means decreased SVR.
Slight increase in HR

6. CV in pregnancy– Big Picture
Pregnancy will make stenotic lesions more symptomatic.
Patient may need interventional procedure (valvuloplasty) or termination of pregnancy.

7. Aortic stenosis at rest
Pulmonary capillaries
LV dilation / hypertrophy
Tricuspid
Aortic stenosis
Mitral
Pulmonic
Aortic stenosis at rest
Cardiac output not sufficient to cause critically high LV intracavitary pressure / LV failure.
Resistance arterioles

8. 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

9. CV in pregnancy– Big Picture
AI and MR are often well tolerated in pregnancy. Decreased SVR helps forward flow.

10. 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”

11. 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.

12. 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.

13. 30-50% of congenital heart patients will have an ASD as part of their disease complex.
home.cc.umanitoba.ca/~soninr/PS.html

14. 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.

15. Dilated collaterals in coarctation
www-clinpharm.medschl.cam.ac.uk/.../index.html

16. Descending thoracic aortic coarctation repaired with stent

17. Tetralogy of Fallot

19. Marcus JT

20. Dong SJ. Smith ER. Tyberg JV
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): , 1992 Oct.

21. 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.

22. 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).

23. 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.

24. 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).

25. 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.

26. Eisenmenger’s syndrome with pulmonary artery hypertrophy.
Patient is thin, cyanotic and may have clubbing.
tchin.org/portraits/angela-1.htm

27. 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).

28. 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

29. Pulmonary hypertension—
What causes it?
Exactly how does it kill patients?

30. 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)

31. 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.

32. Passive Influences on PVR: Capillary Recruitment and Distension

34. Pulmonary hypertension
Acute pulmonary thromboembolism

35. Pulmonary hypertension
Chronic pulmonary thromboembolism

36. 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.

37. 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.

38. 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!

39. Pulmonary hypertension
PA catheter for actual measurement of PA pressure and titration of pulmonary vasodilators.

40. In MS, HOCM and AS Keep HR down
“Slow and tight” for stenotic CV lesions.

41. Pulmonary Hypertension
Specific drug Rx:
Inhaled O2
Inhaled NO
IV, SQ, inhaled, oral: Epoprostenol = prostacyclin = Flo-Lan
Endothelin antagonist: Bosentan (Tracleer)
Oral sildenafil (Viagra).

42. 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.

43. 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.

44. Compensated patient with POTENTIAL RL shunt.LA LV
High SVR,
Minimal RL shunt Ao 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.

45. Decompensated patient with REAL RL shunt.LA LV
Decreased SVR desaturation Ao PA
Increased pulmonary vascular resistance desaturation RA RV
Decompensated patient with ASD, VSD or PDA-- Decreased SVR or increased pulmonary vascular resistance  increased RL shunt and increased arterial desaturation.

46. What lowers SVR? Exercise Spinal or epidural anesthesia.
Vasodilating anesthetics (sevoflurane, isoflurane, desflurane)
Sodium nitroprusside
Hydralazine
Oxytocin
Fever
Squatting RAISES SVR (Tetralogy of Fallot).

47. Repeat CS. Epidural anesthesia
Repeat CS. Epidural anesthesia. Delivery with inc in HR and CO, oxytocin bolus with decrease SVR and BP, increase in CO and SV.
Bolus oxytocin (10 U in this example) dramatically lowers SVR and CO usually increases. CO can increase because volume status is adequate, aortocaval compression has been relieved, and oxytocin, by contracting the uterus, causes autotransfusion.

48. 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.,‡

49. What raises pulmonary vascular resistance?
Alveolar hypoxia
Acidosis
Hypothermia
Crying
Pain (catecholamines)

50. 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