Results
Between February 2020 to October 2020, 40 non-consecutive patients median age 63 years (IQR 55-69), 11 (28%) females, scheduled for elective EP procedures at a single center consented and received dobutamine at the end of the procedure for EPS. The patient demographics and the diagnoses for the procedure indications are listed in Table 1.
There was no significant difference in the change in AVNBCL relative to the SCL and the change in the VABCL relative to the SCL at each incremental dose of dobutamine (Tables 2, 3 and 4, Figures 1 and 2).
The SCL shortened with incremental doses of dobutamine (Table 2, 3, 4, Figure 1). The change only became statistically significant at 10 mcg/kg/min and greater doses. The largest percentage decrease in the SCL from one consecutive dose escalation to the next was noted between 5 and 10 mcg/kg/min. Similarly, antegrade and retrograde AV nodal conduction shortened with each dose of dobutamine and the largest decrease in AVNBCL and VABCL between consecutive dose escalations was also noted between 5 and 10 mcg/kg/min (Table 2, 3, 4, Figures 2). The AH interval shortened at 15 mcg/kg/min and greater doses (Tables 2, 3, 4, Figure 3) but the HV interval did not show evidence of change (Tables 2, 3, 4, Figure 4). As expected, the QRS duration did not change significantly from baseline to each incremental dose of dobutamine (Tables 2, 3, 4, Figure 5). The QT interval decreased with escalation in dobutamine dose starting at 15 mcg/kg/min, an expected finding given that the sinus cycle length decreased with higher doses of dobutamine, and the QT was not corrected for rate (Tables 2, 3, 4, Figure 5).
The effects of dobutamine on the anterograde AVNERP could not be determined consistently because, in many cases, it was shorter than the AERP. The SCL shortened with each dobutamine dose escalation and required shortening of the drive cycle length when measuring effective refractory periods. Shorter drive train cycle length also led to AV nodal block precluding measurement of the AVNERP. AVNERP was not reported when it was shorter than the AERP. The retrograde AVNERP could not be assessed consistently because retrograde conduction was limited by His-Purkinje refractoriness or inability to see a stable retrograde His deflection. The AVNERP data were included in the analysis; however, the results should be viewed in the context of the limitations described above (Table 3, 4, Figure 6). The change in the AVNERP only reached statistical significance at 15 mcg/kg/min and 20 mcg/kg/min.
Although there was no significant decrease in the AERP from baseline up to 15 mcg/kg/min of dobutamine, there was a significant decrease in the AERP from baseline to 20 mcg/kg/min (Tables 2, 3, 4, Figure 6). However, the shortening of the AERP was likely due to shortening of the drive cycle length necessary to avoid competition with the shortening of the SCL. Although there was no significant decrease in the VERP from baseline to 5 mcg/kg/min of dobutamine, there was a significant decrease in the VERP from baseline to 10 mcg/kg/min, to 15 mcg/kg/min and to 20 mcg/kg/min dobutamine (Tables 2, 3, 4, Figure 6). The decrease in the VERP was likely secondary to the necessity of having to decrease the drive train cycle length due to the decrease in SCL with each dose escalation of dobutamine dose.
Changes in diastolic and systolic blood pressure with escalating doses of dobutamine are shown in Tables 2, 3, 4 and Figure 7. The systolic blood pressure increased significantly by 11 mm of Hg to a maximum at 15 mcg/kg/min and then decreased slightly at 20 mcg/kg/min. The diastolic blood pressure decreased significantly by 8 mm Hg to a minimum at 20 mcg/kg/min.
Three patients had no retrograde conduction at baseline. One patient developed retrograde conduction at 5 mcg/kg/min of dobutamine, one patient at 20 mcg/kg/min, and one patient had no retrograde conduction during the study.
Four patients (10%) were hypotensive, defined as systolic blood pressure <90 mmHg, at baseline (87, 83, 86, and 84), secondary to the effects of sedation. All four patients were able to tolerate dobutamine with no limitations. Hypotensive episodes were recorded in two additional patients (5%), a total of six patients (15%), during the study but none required a vasopressor nor subsequently developed end organ damage as a result. Another patient (2.5%) received a vasopressor for systolic blood pressure in the 90s based on the discretion of the anesthesiologist during 15 mcg/kg/min of dobutamine infusion and the dobutamine dose was not increased to 20 mcg/kg/min. One patient (2.5%) developed junctional rhythm at 20 mcg/kg/min of dobutamine but remained normotensive.
One patient (2.5%) developed atrial fibrillation at 10 mcg/kg/min and another patient (2.5%) developed AVNRT at 15 mcg/kg/min. For both patients, dobutamine was held and subsequently tolerated ablation with no further adverse events.
We did not perform ventricular pacing for VABCL or VERP in 13 patients who underwent AF ablations given the length of the procedure and the effect of ventricular pacing on the blood pressure.