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.