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[Effect of defibrillation on hemodynamics during cardioverter defibrillator implantation]
1Department of Cardiovascular Surgery, Heart Institute of Japan, Tokyo Women's Medical College.
Insights
Repeated defibrillation can worsen hemodynamics in patients with poor ventricular contractility. Patients with reduced left ventricular function experienced sustained negative hemodynamic effects after defibrillation during cardioverter defibrillator implantation.
Area of Science:
- Cardiovascular Physiology
- Electrophysiology
- Medical Device Technology
Context:
- Malignant ventricular arrhythmias necessitate cardioverter defibrillator implantation.
- Hemodynamic assessment is crucial during device implantation procedures.
- Ventricular fibrillation and defibrillation significantly impact cardiac function.
Purpose:
- To evaluate the hemodynamic effects of induced ventricular fibrillation and defibrillation in patients undergoing cardioverter defibrillator implantation.
- To compare these effects between patients with different levels of ventricular contractility.
Summary:
- Fifteen patients were divided into two groups based on preoperative left ventricular fractional shortening (<0.20 and >0.20). Hemodynamic parameters including mean blood pressure, cardiac output, and left ventricular stroke work index were measured before and after defibrillation.
- Patients with poor ventricular contractility (Group A) showed consistently lower postoperative hemodynamic values and a greater decrease in end-systolic wall stress after defibrillation compared to those with better contractility (Group B).
- Group A exhibited a more drastic increase in rate-corrected mean velocity of circumferential fiber shortening post-defibrillation, suggesting impaired recovery. These findings indicate that repeated defibrillations may deteriorate hemodynamics in patients with compromised ventricular function.
Impact:
- These findings highlight the potential risks of repeated defibrillation in patients with poor ventricular contractility.
- The study suggests that the left ventricle's intolerance to abrupt hemodynamic changes during fibrillation and defibrillation contributes to adverse outcomes.
- Understanding these hemodynamic influences is vital for optimizing patient management and device programming in electrophysiology.
Abstract:
This study evaluated the influences of induced ventricular fibrillation and defibrillation on the hemodynamics in patients with malignant ventricular arrhythmias during cardioverter defibrillator implantation. A total of 15 patients were analyzed, divided into 2 groups based on ventricular contractility. Group A included 6 patients with preoperative left ventricular fractional shortening < or = 0.20 and Group B consisted of 9 patients with fractional shortening > 0.20. Mean blood pressure, cardiac output, pulmonary capillary wedge pressure, and left ventricular stroke work index were measured before and after ventricular fibrillation and defibrillation. In addition, end-systolic wall stress and rate-corrected mean velocity of circumferential fiber shortening were obtained from transesophageal echocardiography. In Group B, measured 30 sec after defibrillation, mean blood pressure, cardiac output, and left ventricular stroke work index increased significantly (p < 0.05), whereas only pulmonary capillary wedge pressure indicated a significant increase (p < 0.001) after defibrillation in Group A. Throughout 5 repeated ventricular fibrillations and defibrillations. Group A showed consistently lower postoperative values than preoperative values for mean blood pressure, cardiac output and left ventricular stroke work index. In contrast, in Group B, the postoperative values were constantly higher than preoperative values. Although end-systolic wall stress decreased after defibrillation in both groups, the magnitude of decrease was significantly greater in Group A than in Group B (p < 0.01). While rate-corrected mean velocity of circumferential fiber shortening increased after defibrillation in both groups, the difference of rate-corrected mean velocity of circumferential fiber shortening between Groups A and B was statistically significant at beats one and 2 following defibrillation (p < 0.05) where Group A indicated a more drastic increase than Group B. In both groups, post-defibrillation end-systolic wall stress and rate-corrected mean velocity of circumferential fiber shortening gradually approached the preoperative values as beats proceeded. These results suggest that repeated defibrillations in patients with poor ventricular contractility potentially deteriorates hemodynamics, presumably because the left ventricle is often intolerant to abrupt arterial collapse by ventricular fibrillation and to subsequent rapid preload increase after defibrillation.