Fetal cardiac bypass using an in-line axial flow pump to minimize extracorporeal surface and avoid priming volume.
BACKGROUND
Progressive metabolic acidosis, hypoxia, and hypercarbia develop rapidly after fetal cardiac bypass mainly as a result of an increase in placental vascular resistance and a decrease in placental blood flow. A number of factors including fetal stress, priming substances, and extracorporeal surfaces have been identified as possible stimuli causing this placental dysfunction. The purpose of this study was to examine the effects of avoiding priming volume and minimizing extracorporeal surface area on placental hemodynamics and function.


METHODS
Fetal sheep (n = 16) at 118 to 122 days of gestation were subjected to cardiac bypass for 30 minutes using either an in-line axial-flow pump (Hemopump group: n = 8, no prime) or a roller pump with a venous reservoir (control group: n = 8, priming volume = 150 mL). After bypass, the fetuses were observed for 90 minutes. Placental blood flow and combined ventricular output were continuously measured with ultrasonic flow probes, and fetal blood gases were measured at specific intervals.


RESULTS
Three fetuses in the control group died during the study, whereas all 8 fetuses in the Hemopump group remained in stable condition throughout the study period. During and after bypass, placental blood flow was significantly higher (p < 0.0001) and placental vascular resistance was significantly lower (p < 0.0001) in the Hemopump group than in the control group. Arterial pH and partial pressure of arterial oxygen declined significantly less (p < 0.0001), and partial pressure of arterial carbon dioxide increased significantly less (p = 0.0002) in the Hemopump group than in the control group.


CONCLUSIONS
Reducing the extracorporeal surface area and avoiding external priming substances preserves placental hemodynamics after fetal cardiac bypass. An in-line axial-flow pump is useful in miniaturizing the bypass circuits for potential use in fetal cardiac surgery.
Reddy
V M
VM
Division of Cardiothoracic Surgery, University of California, San Francisco 94143-0118, USA.
Liddicoat
J R
JR
Klein
J R
JR
McElhinney
D B
DB
Wampler
R K
RK
Hanley
F L
FL
D000138:Acidosis / Q000209:etiology; D000818:Animals; D002245:Carbon Dioxide / Q000097:blood; D004867:Equipment Design; D005112:Extracorporeal Circulation / Q000009:adverse effects / Q000295:instrumentation*; D005260:Female; D005312:Fetal Blood / Q000737:chemistry; D005315:Fetal Diseases / Q000209:etiology; D005333:Fetus / Q000601:surgery*; D006863:Hydrogen-Ion Concentration; D006935:Hypercapnia / Q000209:etiology; D000860:Hypoxia / Q000209:etiology; D008904:Miniaturization; D010100:Oxygen / Q000097:blood; D010920:Placenta / Q000098:blood supply / Q000000981:diagnostic imaging / Q000502:physiology*; D011247:Pregnancy; D012039:Regional Blood Flow; D012756:Sheep; D013312:Stress, Physiological / Q000503:physiopathology; D013318:Stroke Volume; D013499:Surface Properties; D015996:Survival Rate; D014463:Ultrasonography; D014655:Vascular Resistance; D016276:Ventricular Function
D002245:Carbon Dioxide; D010100:Oxygen