Ulrich Achleitner

A fast and compact quantum random number generator

We present the realization of a physical quantum random number generator based on the process of splitting a beam of photons on a beam splitter, a quantum mechanical source of true randomness. By utilizing either a beam splitter or a polarizing beam splitter, single photon detectors and high speed electronics the presented devices are capable of generating a binary random signal with an autocorrelation time of 11.8 ns and a continuous stream of random numbers at a rate of 1 Mbit/s. The randomness of the generated signals and numbers is shown by running a series of tests upon data samples. The devices described in this paper are built into compact housings and are simple to operate.

The effects of repeated doses of vasopressin or epinephrine on ventricular fibrillation in a porcine model of prolonged cardiopulmonary resuscitation.

This study evaluated ventricular fibrillation mean frequency and amplitude to predict defibrillation success in a porcine cardiopulmonary resuscitation (CPR) model using repeated administration of vasopressin or epinephrine. After 4 min of cardiac arrest and 3 min of CPR, 10 pigs were randomly assigned to receive either vasopressin (early vasopressin: 0.4, 0.4, and 0.8 units/kg, respectively, n = 5) or epinephrine (early epinephrine: 45, 45, and 200 &mgr;g/kg, respectively, n = 5). Another 11 animals were randomly allocated after 4 min of cardiac arrest and 8 min of CPR to receive every 5 min either vasopressin (late vasopressin: 0.4 and 0.8 units/kg, respectively, n = 5) or epinephrine (late epinephrine: 45 and 200 &mgr;g/kg, n = 6). Ventricular fibrillation mean frequency and amplitude on defibrillation were significantly higher in the vasopressin groups than in the epinephrine groups, respectively. In vasopressin versus epinephrine animals, mean frequency immediately before defibrillation was 9.6 ± 1.5 Hz vs 7.0 ± 0.7 Hz (P < 0.001), mean amplitude was 0.65 ± 0.26 mV vs 0.21 ± 0.14 mV (P < 0.001, and coronary perfusion pressure was 27 ± 9 mm Hg vs 8 ± 4 mm Hg (P < 0.00001), respectively. In contrast to no epinephrine animals, all vasopressin animals were successfully defibrillated and survived 1 h (P < 0.05). Mean fibrillation frequency and amplitude predicted successful defibrillation and may serve as noninvasive markers to monitor continuing CPR efforts. Furthermore, vasopressin was superior to epinephrine in maintaining these variables above a threshold necessary for successful defibrillation. Implications Mean frequency and amplitude of ventricular fibrillation predicted successful defibrillation in pigs. Vasopressin was superior to epinephrine in maintaining these variables above a success defibrillation threshold.

Analysing ventricular fibrillation ECG-signals and predicting defibrillation success during cardiopulmonary resuscitation employing N(α)-histograms

Mean fibrillation frequency may predict defibrillation success during cardiopulmonary resuscitation (CPR). N(alpha)-histogram analysis should be investigated as an alternative. After 4 min of cardiac arrest, and 3 versus 8 min of CPR, 25 pigs received either vasopressin or epinephrine (0.4, 0.4, and 0.8 U/kg vasopressin versus 45, 45, and 200 microg/kg epinephrine) every 5 min with defibrillation at 22 min. Before defibrillation, the N(alpha)-parameter histogramstart/histogramwidth and the mean fibrillation frequency in resuscitated versus non-resuscitated pigs were 2.9+/-0.4 versus 1.7+/-0.5 (P=0.0000005); and 9.5+/-1.7 versus 6.9+/-0.7 (P=0.0003). During the last minute prior to defibrillation, histogramstart/histogramwidth of > or =2.3 versus mean fibrillation frequency > or =8 Hz predicted successful defibrillation with subsequent return of a spontaneous circulation for more than 60 min with sensitivity, specificity, positive predictive value and negative predictive value of 94 versus 82%, 96 versus 89%, 98 versus 93% and 90 versus 74%, respectively. We conclude, that N(alpha)-analysis was superior to mean fibrillation frequency analysis during CPR in predicting defibrillation success, and distinction between vasopressin versus epinephrine effects.

The Efficacy of Epinephrine or Vasopressin for Resuscitation During Epidural Anesthesia

Cardiopulmonary resuscitation (CPR) during epidural anesthesia is considered difficult because of diminished coronary perfusion pressure. The efficacy of epinephrine and vasopressin in this setting is unknown. Therefore, we designed this study to assess the effects of epinephrine versus vasopressin on coronary perfusion pressure in a porcine model with and without epidural anesthesia and subsequent cardiac arrest. Thirty minutes before induction of cardiac arrest, 16 pigs received epidural anesthesia with bupivacaine while another 12 pigs received only saline administration epidurally. After 1 min of untreated ventricular fibrillation, followed by 3 min of basic life-support CPR, Epidural Animals and Control Animals randomly received every 5 min either epinephrine (45, 45, and 200 &mgr;g/kg) or vasopressin (0.4, 0.4, and 0.8 U/kg). During basic life-support CPR, mean ± sem coronary perfusion pressure was significantly lower after epidural bupivacaine than after epidural saline (13 ± 1 vs 24 ± 2 mm Hg, P < 0.05). Ninety seconds after the first drug administration, epinephrine increased coronary perfusion pressure significantly less than vasopressin in control animals without epidural block (42 ± 2 vs 57 ± 5 mm Hg, P < 0.05), but comparably to vasopressin after epidural block (45 ± 4 vs 48 ± 6 mm Hg). Defibrillation was attempted after 18 min of CPR. After return of spontaneous circulation, bradycardia required treatment in animals receiving vasopressin, especially with epidural anesthesia. Systemic acidosis was increased in animals receiving epinephrine than vasopressin, regardless of presence or absence of epidural anesthesia. We conclude that vasopressin may be a more desirable vasopressor for resuscitation during epidural block because the response to a single dose is longer lasting, and acidosis after multiple doses is less severe compared with epinephrine.

The beneficial effect of basic life support on ventricular fibrillation mean frequency and coronary perfusion pressure

BACKGROUND AND OBJECTIVE Chest compressions before initial defibrillation attempts have been shown to increase successful defibrillation. This animal study was designed to assess whether ventricular fibrillation mean frequency after 90 s of basic life support cardiopulmonary resuscitation (CPR) may be used as an indicator of coronary perfusion and mean arterial pressure during CPR. METHODS AND RESULTS After 4 min of ventricular fibrillation cardiac arrest in a porcine model, CPR was performed manually for 3 min. Mean ventricular fibrillation frequency and amplitude, together with coronary perfusion and mean arterial pressure were measured before initiation of chest compressions, and after 90 s and 3 min of basic life support CPR. Increases in fibrillation mean frequency correlated with increases in coronary perfusion and mean arterial pressure after both 90 s (R=0.77, P<0.0001, n=30; R=0.75, P<0.0001, n=30, respectively) and 3 min (R=0.61, P<0.001, n=30; R=0.78, P<0.0001, n=30, respectively) of basic life support CPR. Increases in fibrillation mean amplitude correlated with increases in mean arterial pressure after both 90 s (R=0.46, P<0.01; n=30) and 3 min (R=0.42, P<0.05, n=30) of CPR. Correlation between fibrillation mean amplitude and coronary perfusion pressure was not significant both at 90 s and 3 min of CPR. CONCLUSIONS In this porcine laboratory model, 90 s and 3 min of CPR improved ventricular fibrillation mean frequency, which correlated positively with coronary perfusion pressure, and mean arterial pressure.

The Prediction of Defibrillation Outcome Using a New Combination of Mean Frequency and Amplitude in Porcine Models of Cardiac Arrest

We estimated the predictive power with respect to defibrillation outcome of ventricular fibrillation (VF) mean frequency (FREQ), mean peak-to-trough amplitude (AMPL), and their combination. We examined VF electrocardiogram signals of 64 pigs from 4 different cardiac arrest models with different durations of untreated VF, different durations of cardiopulmonary resuscitation, and use of different drugs (epinephrine, vasopressin, N-nitro-l-arginine methyl ester, or saline placebo). The frequency domain was restricted to the range from 4.33 to 30 Hz. In the 10-s epoch between 20 and 10 s before the first defibrillation shock, FREQ and AMPL were estimated. We introduced the survival index (SI; 0.68 Hz−1 · FREQ + 12.69 mV−1 · AMPL) by use of multiple logistic regression. Kruskal-Wallis nonparametric one-way analysis was used to analyze the different porcine models for significant difference. The variables FREQ, AMPL, and SI were compared with defibrillation outcome by means of univariate logistic regression and receiver operating characteristic curves. SI increased predictive power compared with AMPL or FREQ alone, resulting in 89% sensitivity and 86% specificity. The probabilities of predicting defibrillation outcome for FREQ, AMPL, and SI were 0.85, 0.89 and 0.90, respectively. FREQ, AMPL, and SI values were not sensitive in regard to the four different cardiac arrest models but were significantly different for vasopressin and epinephrine animals.

Algorithms to analyze ventricular fibrillation signals.

Prediction of the success of defibrillation to avoid myocardial injury and performance feedback during CPR requires algorithms to analyze ventricular fibrillation signals. This report reviews investigations on different parameters of ventricular fibrillation electrocardiographic signals, including amplitude, frequency, bispectral analysis, amplitude spectrum area, wavelets, nonlinear dynamics, N(&agr;) histograms, and combinations of several of these parameters. To date, no satisfactory methods have been found that cope with CPR artifacts and show adequate predictive power of successful defibrillation. The usual limitations of the studies are the small number of subjects, which precludes separation into training and test data. Because many investigations are animal studies of untreated short ventricular fibrillation, the results may be different for prolonged ventricular fibrillation in humans. The universality of threshold values has to be examined, and promising new parameters have to be monitored over longer time periods and analyzed for the effects of chest compressions, ventilation, and concomitant vasopressor therapy.

Waveforms of external defibrillators: analysis and energy contribution

BACKGROUND AND OBJECTIVE Defibrillation is the most important therapy for terminating ventricular fibrillation in cardiac arrest patients. In addition to performing defibrillation at the earliest possible time, appropriate pulse energy and optimal waveform seem to be crucial for success. Emergency medical service personnel use different defibrillators and rely on their similarity of energy content. This study examined the true pulse energy content and waveform of 17 commonly used defibrillators. METHODS AND RESULTS Defibrillation energies were selected to be 30, 200 or 360 J and defibrillators were discharged into test resistors, simulating transthoracic impedances of 25, 50 or 100 Ohms. Pulse energy deviated by up to +23% or -29% from the selected energy. Pulse energy within the initial 8 ms ranged from 90 to 30% of total pulse energy. Fourteen defibrillators utilising damped sinusoidal waveforms produced a monophasic pulse when discharged into resistances of 50 Ohms and 100 Ohms. CONCLUSIONS Defibrillators used at the same energy settings do not necessarily produce the same defibrillation pulse energy. All but one defibrillator actually use monophasic waveforms, leaving the potential advantage of biphasic waveforms unused. Energy accuracy of defibrillators needs to be improved, and biphasic waveforms should be used more.

Corrigendum to “Waveforms of external defibrillators: analysis and energy contribution”

The authors regret the inaccurate measurement of the energy content of the waveform of the Hewlett–Packard/Heartstream Forerunner defibrillator. This happened due to a little known measurement problem concerning the Impulse 3000 Defibrillator Analyser (Dynatech Nevada Inc., Nevada, US) with firmware version 1.10. Using this firmware, energy content of biphasic exponential defibrillator waveforms may be measured incorrectly due to a filtering technique based on waveform specifications as listed in ANSI/ AAMI DF2: 1989 Cardiac Defibrillator Devices document [1]. This could yield energy readings approximately 12% lower than actually delivered energy [2]. The energy of monophasic and damped sinusoidal waveforms is measured correctly. We therefore repeated the measurement of the Hewlett–Packard/Heartstream Forerunner defibrillator waveforms, using a PC based measurement system this time. The waveform is recorded by means of an analog-digital-converter (16 bit amplitude resolution, 20 kHz sampling rate). The defibrillator is discharged into an adjustable resistor (25 to 100 V). Absolute system noise is lower than 91 V. We calculated the total energy of the waveform and the fractional energy delivered within 8 and 40 ms after onset of the waveform using mathematical software (MatLab, The Mathworks, Inc., Natick, MA) (Table 1). All results are given as mean 9 standard deviation of three measurements.

Waveform analysis of biphasic external defibrillators

BACKGROUND AND OBJECTIVE All internal defibrillators and some external defibrillators use biphasic waveforms. The study analysed the discharged waveform pulses of two manual and two semi-automated biphasic external defibrillators. METHODS AND RESULTS The defibrillators were discharged into resistive loads of 25, 50 and 100 Omega simulating the patients transthoracic impedance. The tested biphasic defibrillators differed in initial current as well as initial voltage, varying from 10.9 to 73.3 A and from 482.8 to 2140.0 V, respectively. The energies of the manual defibrillators set at 100, 150 and 200 J deviated by up to +19.1 or -28.9% from the selected energy. Impedance-normalised delivered energy varied from 1.0 to 12.5 J/Omega. Delivered energy, shock duration and charge flow were examined with respect to the total pulse, its splitting into positive and negative phases and their impedance dependence. For three defibrillators pulse duration increased with the resistive load, whereas one defibrillator always required 9.9 ms. All tested defibrillators showed a higher charge flow in the positive phase. Defibrillator capacitance varied between approximately 200 and 100 mu F and internal resistance varied from 2.0 to 7.6 Omega. Defibrillator waveform tilt ranged from -13.1 to 61.4%. CONCLUSIONS The tested defibrillators showed remarkable differences in their waveform design and their varying dependence on transthoracic impedance.