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Perfusion Policies 101: Perfusion & the Pregnant Patient


Editor’s Note:



Welcome to PERFUSION POLICIES 101.  This will be a continuing series provided to assist your programs with that one puzzle piece we all run into now and then- that one time that an unexpected patient condition may give you pause…

The intention here is to disseminate some basic recipes that have probably been implemented at countless institutions, for God knows how long.  The usual disclaimers obviously apply:

Due Diligence is the Responsibility of the Reader!

Use the information as you feel fit, recognizing that this is information gleaned from multiple sources, it is recruited from the public domain of the internet, with no implied assurance of accuracy- but is cogent, and based on logical and reasonable clinical rationale.

Frank Aprile

Perfusion & the Pregnant Patient


Two general categories of heart disease in pregnant women:

  1. Women who have heart disease before pregnancy.
  2. valvular
  3. congenital
  4. coronary artery disease; rare in woman of child-bearing years
  5. severe insulin-dependent diabetes mellitus
  6. genetic hepercholesterolemia
  7. Woman who have heart disease induced by pregnancy.
  8. preeclampsia
  9. cardiomyopathy
  10. thromboembolic disease
  11. aortic dissection

Associated with Low Rates of Maternal Complications But High Risk to the Fetus


  1. Cardiac output increases by 30-50% by the beginning of the third trimester, primarily due to stroke volume rather than heart rate.
  2. Oxygen consumption increases by 10-15%.
  3. Plasma volume increases 50-75%, but red blood cell volume increases only 40-50%, so the patient will seem anemic (estrogen mediated).


  1. Both fetal heart rate and uterine contraction monitors provide valuable information for intraoperative management. Rate can be managed at either normothermia or mild hypothermia.  A decrease in heart rate is associated with poor fetal perfusion.
  2. The woman should be positioned in a left lateral tilt to avoid compression of the inferior vena cava or aorta.
  3. Extracorporeal circuit should be able to accommodate a large blood volume, but employ a minimal priming volume.
  4. Heparinization is well tolerated because the molecule is large and does not cross the placental blood barrier. Pregnancy tends to induce a hypercoagulable state with increases in factors VII, VIII, X, AND XIII,  as well as an increase in blood volume and metabolism.  Theoretically, there should be and increase in heparin requirements.  Therefore, a heparin assay should be done to determine a base requirement,a dn then ACTs should be monitored more frequently.
  5. Mixed venous saturation will measure adequace of perfusion.
  6. Temperature should no fall below 32 degrees centrifrade to avoid fetal fibrillation.
  7. Uteine contractions are associated with hypothermia and rewarming.
  8. Normal fetal heart rate is 120-140 beats/min. Maximize blood flow before giving vasopressors to eachieve pressures of 60-70 mmHg.  Ephedrine is recommended during pregnancy with indirect alpha and beta adrenergic activity.  It appears to have the least effect on uterine blood flow due to the beta – 2 stimulation.
  9. Metabolic acidosis is treated with sodium bicarbonate.
  10. Glucose is given to replenish decreased fetal glycogen stores.
  11. Blood oxygen saturation is corrected by increasing perfusion flow, hemoglobin concentration, or oxygen flows, as indicated.
  12. Note: sodium nitroprusside crosses the placenta in animals, it may liverate free cyanide ions and result in metabolic acidosis.

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