Cardiopulmonary Bypass Transiently Inhibits Intraventricular Vortex Ring Formation in Patients Undergoing Coronary Artery Bypass Graft Surgery

OBJECTIVE:

Transmitral blood flow during early left ventricular (LV) filling produces an intraventricular rotational body of fluid known as a “vortex ring” that enhances the hydraulic efficiency of early LV filling. The authors tested the hypothesis that exposure to cardiopulmonary bypass (CPB) attenuates intraventricular vortex formation time (VFT) in patients with normal preoperative LV systolic and diastolic function undergoing coronary artery bypass graft (CABG) surgery.

DESIGN:

A prospective, observational study.

PARTICIPANTS:

Ten men (65 ± 4 years, 91 ± 11 kg, and 175 ± 8 cm) with a normal preoperative LV ejection fraction (58% ± 6%) scheduled for elective CABG surgery were studied after institutional review board approval.

INTERVENTIONS:

None.

MEASUREMENTS AND MAIN RESULTS:

Anesthesia was induced with etomidate, fentanyl, and rocuronium and maintained with isoflurane. Myocardial protection during CPB consisted of antegrade and retrograde cold blood cardioplegia administered at 15-minute intervals, systemic and topical hypothermia, and warm continuous antegrade cardioplegia before aortic cross-clamp removal. The peak early LV filling and atrial systole blood flow velocities (E and A, respectively) and corresponding velocity-time integrals (VTI-E and VTI-A, respectively) were obtained with pulse-wave Doppler echocardiography and used to determine E/A and atrial filling fraction (β, VTI-A/[VTI-E + VTI-A]), respectively. Mitral valve diameter (D) was calculated as the average of minor and major axis lengths obtained in the midesophageal bicommissural and long-axis transesophageal echocardiographic imaging planes, respectively. VFT was calculated 30 minutes before and 15, 30, and 60 minutes after CPB as 4 × (1 – β) × stroke volume (SV)/πD(3), where SV is the stroke volume measured using thermodilution. All patients separated from CPB in sinus rhythm without pacing or vasoactive drug support. Systemic and pulmonary hemodynamics were similar before compared with all times after CPB. CPB significantly (p < 0.05) reduced VFT (5.3 ± 1.8 to 4.0 ± 1.5 15 minutes after CPB); the recovery of VFT (to 4.7 ± 1.6, p > 0.05 v baseline) was noted 60 minutes after CPB. A reduction in E/A (1.26 ± 0.22 to 0.96 ± 0.27) and an increase in β (0.33 ± 0.04 to 0.41 ± 0.07) occurred 15 minutes after CPB. E/A and β also recovered gradually toward control values after CPB (1.25 ± 0.22 and 0.36 ± 0.04, respectively, 60 minutes after CPB; p > 0.05 v. baseline).

CONCLUSIONS:

The results indicated that CPB transiently attenuate VFT in patients with normal preoperative LV systolic and diastolic function undergoing CABG surgery. These data suggest that CPB adversely affects diastolic transmitral flow efficiency by reducing intraventricular vortex ring formation in vivo.