Sawtooth First Phase Biphasic Defibrillation Waveform

"Sawtooth First Phase" Biphasic Waveform. Introduction : A major limitation in a conventional truncated exponential waveform is the rapid drop in current that results in short duration of high current or longer duration with a lower average current. We hypothesized that increasing the first phase average current by boosting the decaying waveform prior to phase reversal may improve defibrillation efficacy.
Methods and Results : To better simulate a "rectangular" waveform during the first phase, a "sawtooth" defibrillation waveform was constructed using "parallel-series" switching of capacitances (each 30 μF) during the first phase. This permitted a boost in the voltage late in the first phase. This sawtooth hiphasic waveform (sawtooth) was compared to two clinical waveforms: a 135-μF capacitance (control-1) and a 90-μF capacitance (control-2) waveform. Defibrillation threshold (DFT) parameters were evaluated in 13 anesthetized pig models using a system consisting of a transvenous right ventricular apex lead (anode) and a left pectoral ldquo;hot can" electrode (cathode) system. DFT was determined by a "down-up down-up" protocol. The stored energy for sawtooth, control-1, and control-2 was 10.5 ± 2.8 J, 12.3 ± 3.7 J*, and 12.2 ± 2.8 J*, respectively (*P < 0.01 vs sawtooth). The average current of the first phase for sawtooth, control-1, and control-2 was 7.6 ± 1.3 A, 4.7 ± 0.9 A*, and 6.2 ± 0.9 A*, respectively (*P = 0.0001 vs sawtooth).
Conclusion : A sawtooth biphasic waveform utilizing a "parallel-series" switching system of smaller capacitors can improve defibrillation efficacy. A higher average current in the first phase generated by such a waveform may contribute to more efficient defibrillation by facilitating myocyte capture.     

Usefulness of Plasma Catecholamines During Head-Up Tilt as a Measure of Sympathetic Activation in Vasovagal Patients

Vasovagal syncope is a common clinical disorder which has been traditionally related to a vasovagal reflex precipitated by an initial excess sympathetic stimulation. We hypothesized that the increase in plasma Catecholamines during head-up tilt is more accentuated in patients with tilt induced vasovagal syncope. To test this hypothesis, plasma Catecholamines were measured in supine posture and during head-up tilt in patients with a history suggestive of vasovagal syncope. Of these, 13 had a normal response to tilt (nonvasovagal group; age 41 ± 19 [SD]years) and 11 had a vasovagal response to tilt (vasovagal group; 39 ± 20 years). In the supine posture at rest, plasma epinephrine and norepinephrine were not significantly different between the nonvasovagal and the vasovagal groups (39 ± 28 ng/L vs 46 ± 38 ng/L, P = 0.5792, 335 ± 158 ng/L vs 304 ± 124 ng/L, P = 0.6007, respectively). Furthermore, the tilt induced changes in plasma epinephrine and norepinephrine were not different between the two groups (20 ± 20 ng/L vs 35 ± 55 ng/L, P = 0.3562, 264 ± 158 ng/L vs 242 ± 205 ng/L, P = 0.7724, respectively) suggesting that differences in the hemodynamic response to tilt are not predictable by the supine levels of circulating plasma Catecholamines, and that the extent of plasma catecholamines increase during tilt does not determine the hemodynamic outcome of the tilt test. Since orthostatic changes of plasma Catecholamines could be influenced by volume factors, we assessed plasma renin activity and aldosterone as surrogates of blood volume. Baseline plasma renin activity and aldosterone were not significantly different between the two groups. We conclude that inasmuch as plasma catecholamines reflect the status of sympathetic activity, our data do not support the hypothesis that accentuation of sympathetic activity precedes necessarily the tilt induced vasovagal syncope. However, one should take in consideration that multiple factors may influence catecholamine levels and catecholamines kinetics. A hyperresponsiveness of β-receptors to Catecholamines in patients with vasovagal syncope may be suggested but needs to be tested.